How the war on Cholesterol caused our diabetes epidemic

high-density-lipoprotein-hdl

Cholesterol is a molecule required by every cell of the body in fairly large amounts. It can be easily synthesised by these cells, or taken up by them from LDL and other ApoB lipoproteins, but cannot be broken down. Cholesterol is not soluble in water, and thus must be carried through the blood on lipoprotein particles. When the cholesterol produced or taken up by the cells of the body becomes surplus to requirements it is extracted by HDL (ApoA1 lipoproteins) and carried back to the liver for disposal as bile salts and acids (most of this cholesterol is reabsorbed and recycled, but there is also a variable amount lost in faeces). Reverse cholesterol transport (RCT) is the term used for this extraction of unneeded cholesterol. Here we describe a simplified version of reverse cholesterol transport, how this has been modified by new research into HDL, and we explain the effect of raising or lowering insulin and insulin sensitivity on RCT.

This video gives a good overview of the systems we’ll be describing. (The brain has its own, largely separate cholesterol system which we’ll ignore for now).

Cholesterol and insulin

We have about 30g of cholesterol in our bodies, and synthesise well over a gram a day. Only 10% of this is synthesised in the liver, and even less if we eat cholesterol or have a reduced requirement. Our requirement goes up when we are growing (cells are expanding and new cells being made) and down when we are fasting or losing weight (when fat cells and glycogen cells are shrinking, and autophagic processes are clearing unwanted cells). Thus it makes sense, and helps to keep cholesterol in balance with requirements, that cholesterol synthesis is stimulated by insulin (the fed state hormone) and inhibited by glucagon (the fasting state hormone).[1] An additional check on cholesterol synthesis in the fasting state is the activation of AMPK by the ketone body B-hydroxybutyrate.[2] No surprises then that cholesterol synthesis is found to be increased in type 2 diabetes.[3]

If scientists want to create the early signs of heart disease in animals, they need to feed them doses of cholesterol much larger than the total capacity of the body to make cholesterol.[4] However, Jerry Stamler, one of the founding fathers of the diet heart hypothesis, found in the early 1960’s that animals treated in this way got better when the cholesterol feeding stopped – unless they were given extra insulin.[5] This vital clue was missed in the later rush to change our diets – Jerry Stamler advised the population to avoid egg yolk and replace fat with refined carbs, yet human diets never supplied the amount of cholesterol he fed his animals – unfortunately, the new, modified human diet would start to increase insulin to the high levels seen in those chickens once the diabesity epidemic got underway.

Stamler

Reverse Cholesterol Transport

Fortunately our gut and liver cells make a protein called ApoA1, which the liver turns into something called a nascent HDL particle. Unlike VLDL and the other ApoB particles, which are released from the liver as large, fat and cholesterol laden spheres, HDL is produced in an embryonic state, just a few proteins with little if anything in the way of lipids (lipid-poor ApoA1), and only becomes what we call HDL by performing its cholesterol-gathering role out in the body.

HDLs

If we focus on the cells believed to play the major role in atherosclerosis, macrophages (large immune cells) which can turn into foam cells if they become overloaded with cholesterol, we can see HDL at work. Macrophages clear the blood of infectious agents and damaged particles, and have a particular affinity for oxidised LDL particles (oxLDL).[6] LDL becomes oxidised if it stays in the blood too long (more likely with higher levels or small, dense particles) and is exposed to excessive glucose and fructose levels after meals, or to smoking and other oxidative stressors.[7,8,9] Brown and Goldstein, who won the Nobel Prize for discovering the LDL receptor, estimated that 30-60% of LDL is cleared from circulation by macrophages. (Macrophages exposed to excess insulin increase their uptake of oxLDL by 80%).[10] The oxLDL is then broken down and the cholesterol stored – remember it can’t be broken down. As in other cells, any excess is sent to the surface of the cell, to transporters and other structures that make it available for HDL to pick up, as free cholesterol (cholesterol efflux). If this doesn’t happen for some reason, over a long period, there’s a risk of foam cell formation and atherosclerosis. (Macrophages exposed to excess insulin decrease their efflux of cholesterol to HDL by 25%).[10]

LCAT and esterification

After HDL picks up free cholesterol, this is esterified by an enzyme called lecithin cholesterol acyltransferase (LCAT), making the HDL particle larger. Cholesteryl ester (CE) is cholesterol joined to a fatty acid, usually an unsaturated fatty acid, which is supplied from the phospholipids also picked up from cells by HDL. The more effectively HDL can esterify cholesterol, the sooner it can return to pick up more from the macrophage (or other cell) – this is called HDL efflux capacity – and the phospholipids found in egg yolk have been shown to increase HDL efflux capacity.[11] Phospholipids, found in all whole foods, especially fatty ones like eggs, nuts, seeds, liver, shellfish, and soya beans, are good things to have in your diet; you won’t get them from eating flour, sugar, and oil.

545px-Cholesterol_Oleate

Cholesteryl oleate – a cholesteryl ester

 

CETP – swapping cholesteryl esters for triglycerides

HDL renews itself in the bloodstream by moving cholesteryl esters onto VLDL and other ApoB particles, in more-or-less equal exchange for triglycerides (TGs), through a banana-shaped protein tunnel called Cholesteryl Ester Transport Protein (CETP) which docks between ApoA1 and ApoB particles. HDL can then shed the TGs picked up to help feed cells along its path (as ApoB particles also do), turning them into free fatty acids and glycerol by the action of lipase enzymes. However, the CETP exchange is another place where things can go wrong. If there are too many TGs on VLDL, and too many TG-rich VLDL particles, and fats are not being burned by the body (yes, we’re talking about insulin resistance again), then the piling of TGs onto HDL via CETP will result in its recall to the liver after limited efflux.[12] Carrying lots of TGs back to the liver that made them is not a good use of HDL’s time. And the cholesterol esters being transferred to former TG-rich VLDL is what makes the “Pattern B” lipoproteins, small dense LDL, which are more likely to oxidise and more easily taken up by macrophages. LDL really, once it’s done its job of delivering fat, cholesterol, antioxidants and proteins to cells that need them, ought to be helping in reverse cholesterol transport by ferrying the extra cholesterol esters it received from HDL back to the liver. Large, cholesterol-dense LDL particles – “Pattern A” – are better at this. Small, dense LDL particles aren’t taken up as avidly by the liver, so tend to stay in circulation and oxidize. Hence the TG/HDL ratio is a critical predictor of cardiovascular risk, whether or not we factor in LDL.

The exchange via CETP action is thought responsible for the inverse relationship between levels of TG and HDL-C. Specifically, the larger the VLDL pool (higher TG level), the greater the CETP-mediated transfer of CE from HDL to VLDL in exchange for TG, resulting in TG-rich small, dense HDL which are catabolized more rapidly, leading to low levels of HDL-C. These small, dense HDL also have reduced antioxidant and anti-inflammatory properties. Thus, the greater the increase in hepatic VLDL-TG synthesis and secretion that characterizes insulin-resistant/hyperinsulinemic individuals, the lower will be the HDL-C concentration.[12]

 

Insulin LDL

Insulin resistance in this population (n=103,000) was stratified by tertiles of TG and HDL, with the insulin sensitive tertile having a mean TG/HDL ratio of 1.1 [13]


Fasting, weight loss, and LDL

People who are naturally lean and active and have good insulin sensitivity are at very low risk of cardiovascular disease; they tend to burn fat and have low TG/HDL ratios on any diet. Paradoxically, LDL rises sharply when such people fast for long periods.[14] Despite this, no-one as far as we know has ever suggested that not eating enough causes atherosclerosis. Of course TGs and insulin also fall, while HDL stays the same. But strangely, this rise in LDL does not happen in obese people or people with atherosclerosis.[15]

 

Fasting LDL Apo B

In healthy lean individuals, LDL and ApoB rise as Insulin-like growth factor falls during a fast.[14]

Fasting Chol athero

In obesity or T2DM, or in this case a patient with arteriosclerosis, cholesterol and LDL do not rise during a fast.[15]

Phinney and colleagues found that LDL first fell, then rose significantly, during major weight loss. They calculated that this was due to the delayed removal of around 100g extra cholesterol from the adipose of obese people. LDL became normal when a weight maintenance diet replaced the (low fat, reduced calorie) weight loss diet.[16]
Think about this – all of this extra 100g of cholesterol, 3x the usual whole body content, was eventually removed by reverse cholesterol transport. Some of it ended up on LDL, increasing the LDL count to the level where statins would be indicated according to guidelines. This did not prevent its removal. There is no “LDL gradient” that forces cholesterol back into the body. The LDL level doesn’t tell you whether cholesterol is coming or going – the TG/HDL ratio is the best guide to that.[17]

Lipides

Hepatic lipase – burning fat.

ApoA1 and HDL production increases the release of hepatic lipase, so in a sense ApoA1 is a fat-burning protein, which helps to explain why eating fat increases ApoA1 output.[18, 19] More lipase means lower TGs all round. So, making more HDL can lower TGs, just as making too many TGs can lower HDL – but only the latter is likely to be harmful.

Of course, a low fat, high carbohydrate diet decreases ApoA1, but this doesn’t mean it’s bad if you’re insulin sensitive and have low TGs (and low LDL) eating such a diet, as many people do; the lower lipid circulation all round probably just means that less ApoA1 will be required for equilibrium. However, the old assumption that the lower fat higher carb diet is the “Prudent” diet hasn’t aged well.

We have previously reported that apoA-I and HDL directly affect HL-mediated triacylglycerol hydrolysis, and showed that the rate of triacylglycerol hydrolysis is regulated by the amount of HDL in plasma.

The antioxidant and antiinflammatory benefits of HDL.

Reverse cholesterol transport is the core business of HDL, but it isn’t the only business; HDL is like a busy doctor with a useful bag of healing tricks trundling up and down your bloodstream. For example, HDL carries an antioxidant protein, PON1. When a fatty hamburger meal rich in lipid peroxides was fed to 71 subjects, those with higher HDL experienced a much smaller rise in oxLDL.[20]

The pre-meal HDL level was associated with the extent of the postprandial rise in oxidized LDL lipids. From baseline to 6 h after the meal, the concentration of ox-LDL increased by 48, 31, 24, and 16 % in the HDL subgroup 1, 2, 3, and 4, respectively, and the increase was higher in subgroup 1 compared to subgroup 3 (p = 0.028) and subgroup 4 (p = 0.0081), respectively. The pre-meal HDL correlated with both the amount and the rate of increase of oxidized LDL lipids. Results of the present study show that HDL is associated with the postprandial appearance of lipid peroxides in LDL. It is therefore likely that the sequestration and transport of atherogenic lipid peroxides is another significant mechanism contributing to cardioprotection by HDL.

Tregs or T regulatory cells are a type of immune cell that switches off inflammatory responses. They are also a type of cell that takes up HDL, and HDL selectively promotes their survival. This is a good thing.[21]

Can LDL help in reverse cholesterol transport?

 

The answer is yes – if it’s large LDL particles (Pattern A), not so much small dense ones. Triglycerides and VLDL, on the other hand, are no help at all.

There are two pathways by which RCT can occur. In the first, the scavenger receptor class B type 1 (SRB-1) mediates hepatic uptake of CE from HDL particles without uptake of apoA-I or the whole HDL particle [74]. In the second pathway, cholesteryl ester transfer protein (CETP) catalyzes the transfer of CE from HDL to apoB-containing lipoproteins (VLDL and LDL) in exchange for TG from the apoB-containing lipoproteins (Fig. 1) [21, 75]. This exchange results in apoB-containing lipoproteins which are enriched with CEs and depleted of TGs, and HDL particles which are depleted of CEs and enriched with TGs. The TG-rich and CE-poor HDL particles are catabolized faster than large, CE-rich HDL (apoA-I FCR is increased as noted in Fig. 1), a finding resulting in lower levels of HDL-C in the setting of high TG levels [76]. The apoB-containing lipoproteins, now enriched in CE, can also be taken up by the liver receptors as previously described [75]. When TG levels are high, the apoB particles are TG-enriched and hepatic lipase then hydrolyzes the TGs within the TG-rich LDL to release FFAs, a process which remodels the LDL particles into smaller and denser LDL particles which can enter the arterial intima more easily than larger LDL particles, thus making them more atherogenic (Fig. 1). Small, dense LDL particles also bind less avidly to the LDL receptor, thus prolonging their half-life in the circulation and making these particles more susceptible to oxidative modification and to subsequent uptake by the macrophage scavenger receptors [12].

An unusual experiment (using a radioactive nanoemulsion mimetic of LDL) showed that LDL cholesterol is removed from circulation more rapidly in resistance-trained healthy men than in sedentary healthy men. oxLDL was 50% lower in the resistance-trained men – but total LDL levels were the same, probably as a result of increased beta-oxidation (fat burning).[22]

Why are doctors being confused about HDL and reverse cholesterol transport?

There’s a trend in mainstream medicine to be dismissive of HDL and treat reverse cholesterol transport as unimportant; LDL lowering is the thing. New evidence from genetics, epidemiology, and drug trials is increasingly misinterpreted in this way – probably because drugs that increase HDL have, with some exceptions, been failures. However, drugs that raise HDL, and lower LDL, by inhibiting CETP are not helping either particle do its job; so far, they have neither decreased nor increased the rate of heart attacks in people taking them. Drugs that raise HDL by increasing ApoA1 and nascent HDL output, like the fibrates (e.g. gemfibrozil), do decrease CHD – but only in people with lower HDL and higher TGs! Moderate alcohol use, which also increases ApoA1 output, seems to have a similar effect, though the first randomised controlled trial of this observational hypothesis is only beginning.[23, 24] Even statins help with RCT by decreasing the synthesis of cholesterol in peripheral tissues, thus leaving more room on HDL for efflux cholesterol – again, statins only seem to reduce CHD in the subgroup of people with lower HDL. Clearly reverse cholesterol transport is very important, and efficient reverse cholesterol transport can best explain why so many people with high LDL and high cholesterol do enjoy long lives free from cardiovascular disease. Some ApoA1 genes that especially promote RCT are associated with reduced CVD risk, notably ApoA1 milano – which is actually associated with low HDL, because HDL clearance is so rapid – a paradox which highlights the trickiness of measuring a dynamic process across all tissues only by what appears in the blood.[25] Efficient RCT is associated with lean genes, but it’s largely something you have to work for – eating right, exercising, and looking after yourself in various ways – including giving up smoking, or not starting – which may be why the drug industry has largely given up on it.[26]

We observed that normolipidemic smokers present higher total plasma and HDL phospholipids (PL) (P < .05), 30% lower postheparin hepatic lipase (HL) activity (P < .01), and 40% lower phospholipid transfer protein (PLTP) activity (P < .01), as compared with nonsmokers. The plasma cholesteryl ester transfer protein (CETP) mass was 17% higher in smokers as compared with controls (P < .05), but the endogenous CETP activity corrected for plasma triglycerides (TG) was in fact 57% lower in smokers than in controls (P < .01). Lipid transfer inhibitor protein activity was also similar in both groups. In conclusion, the habit of smoking induces a severe impairment of many steps of the RCT system even in the absence of overt dyslipidemia.


The latest study on very, very high HDL – why isn’t it good?

Last year we wrote about the CANHEART study, which seemed to show adverse health effects of higher HDL. We wrote then that this was probably showing an effect of alcoholism, hereditary CETP defects, and other factors, and not an increase in heart disease. A new study allows us to look at this problem in more detail.[27]

When compared with the groups with the lowest risk, the multifactorially adjusted hazard ratios for all-cause mortality were 1.36 (95% CI: 1.09–1.70) for men with HDL cholesterol of 2.5–2.99 mmol/L (97–115 mg/dL) and 2.06 (1.44–2.95) for men with HDL cholesterol ≥3.0 mmol/L (116 mg/dL). For women, corresponding hazard ratios were 1.10 (0.83–1.46) for HDL cholesterol of 3.0–3.49 mmol/L (116–134 mg/dL) and 1.68 (1.09–2.58) for HDL cholesterol ≥3.5 mmol/L (135 mg/dL).

Those are some very high HDL levels, and not surprisingly fewer than 4% of men and even fewer women had HDL levels so high that they were associated with any extra risk.
Compare that with 40% of both men and women having low HDL levels that were associated with an equally elevated risk!
Further, the risk associated with very high HDL, though it does include cardiovascular deaths, doesn’t seem to include much increased risk of heart attacks and strokes.

VVHi HDL

This is consistent with alcoholism (a confounder not measurable with accuracy, as we described in the CANHEART analysis) increasing deaths from heart failure, cancer, and other causes, and with no further benefit (but maybe not much harm overall) from CETP variants elevating HDL.[28] Furthermore, interactions between heavy alcohol consumption and genes associated with higher HDL have been noted in some populations.[29]
Note that the HDL level associated with lowest heart disease and stroke incidence in this study is well to the right of the bell curve of population HDL distribution. Most of these people could have done with more HDL.
Madsen et al discuss their results soberly; although they fail to discuss the potential role of alcohol, which would explain the exact pattern of increased mortality seen well, and don’t highlight the 10-fold larger impact associated with low HDL in their study, there is nothing biased about their analysis. The European Heart Journal’s editorial was also worth reading.[30]

HDL

However, as reported in medical media, the message changed a bit.

“It appears that we need to remove the focus from HDL as an important health indicator in research, at hospitals and at the general practitioner. These are the smallest lipoproteins in the blood, and perhaps we ought to examine some of the larger ones instead. For example, looking at blood levels of triglyceride and LDL, the ‘bad’ cholesterol, are probably better health indicators,” he notes.

Well yes, looking at everything is good, and TGs and the TG/HDL ratio as well as LDL will give you extra information about the likely reasons for low HDL and whether you need to worry about it. However, Denmark, where the extremely high HDL study was done, is a place where high LDL (the ‘bad’ cholesterol, remember) is associated with lower all-cause mortality in those over 50 free from diabetes or CVD at the start of the study.[31] Over 50 is when most CVD and type 2 diabetes is diagnosed, so LDL might not be all that informative unless you can look at the subclasses of oxLDL, sdLDL, particle number, and so on (of course part of the effect of LDL in Denmark will be due to that country’s higher dairy fat intake, which will also raise HDL and LDL particle size, maybe helping to explain why the association is so favourable in that population).

If we look at the PURE study, higher fat consumption is associated with both higher LDL and higher ApoA1 and HDL, with saturated fat (like all fat types) tending to improve the ApoB/ApoA1 ratio.[32] This is consistent with many other lines of evidence.

Intake of total fat and each type of fat was associated with higher concentrations of total cholesterol and LDL cholesterol, but also with higher HDL cholesterol and apolipoprotein A1 (ApoA1), and lower triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein B (ApoB) to ApoA1 (all ptrend<0·0001).

This is just what fat-burning does, and there’s maybe not a lot of reason to think it’s good or bad per se. What is good about it is, that fat burning lowers insulin. Insulin is what makes your cells hoard cholesterol, and it’s also one of the things that can mess with reverse cholesterol transport. If you’re making or using excess insulin, the switch to a fat burning metabolism allows the insulin to normalise and causes your cells, including the macrophages, to let go of cholesterol – and when they do, the lipoproteins are there ready to carry it away.

Takeaways

Reverse cholesterol transport manages cholesterol flux through all cells and helps us reach a healthy old age.

LDL cholesterol is not a reliable guide to the state of cholesterol flux unless TG/HDL (and HbA1c) are factored in as well. LDL may increase when cholesterol is being removed or in states where it is not being taken up by cells.

Reverse cholesterol transport can remove prodigious amounts of cholesterol from the body during weight loss.

Excessive triglycerides due to insulin resistance can impair reverse cholesterol transport, as can smoking.

Various nutritional factors found in whole food diets have been found to assist in reverse cholesterol transport (including phospholipids, CLA, and polyphenols).

HDL in the high (if not the “extremely high”) range usually correlates with efficient reverse cholesterol transport and has benefits for cardiovascular health, inflammation, antioxidant status etc, but people with HDL outside (higher or lower than) the ideal range can be equally healthy if their overall metabolic health (insulin sensitivity) is good.

The TG/HDL ratio is a good measure of insulin sensitivity, and if excessive can be improved by lowering excessive insulin levels. A low carb diet, intermittent fasting, exercise, or weight loss are all effective ways to correct the TG/HDL ratio.

References

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[2] Bae HR, Kim DH, Park MH, et al. β-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation. Oncotarget. 2016;7(41):66444-66454. doi:10.18632/oncotarget.12119.

[3] Gylling H, Hallikainen M, Pihlajamäki J, et al. Insulin sensitivity regulates cholesterol metabolism to a greater extent than obesity: lessons from the METSIM Study. Journal of Lipid Research. 2010;51(8):2422-2427. doi:10.1194/jlr.P006619.

[4] Regulation of hepatic LDL metabolism in the guinea pig by dietary fat and cholesterol.
Lin ECK, Fernandez ML, Tosca MA, McNamara DJ. Journal of Lipid Research. 1994; 35:446-457

[5] Stamler J, Pick R, Katz LN. Effect of Insulin in the Induction and Regression of Atherosclerosis in the Chick. Circulation Research. 1960; 8:572-576.
Stamler Chick

[6] Brown MS, Goldstein JL. Lipoprotein Metabolism in the Macrophage: Implications for Cholesterol Deposition in Atherosclerosis. Annual Review of Biochemistry 1983 52:1, 223-261
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[7] Kopprasch S, Pietzsch J, Kuhlisch E et al. In Vivo Evidence for Increased Oxidation of Circulating LDL in Impaired Glucose Tolerance. Diabetes 2002; 51(10): 3102-3106. https://doi.org/10.2337/diabetes.51.10.3102

[8] Vos MB, Weber MB, Welsh J et al. Fructose and Oxidized LDL in Pediatric Nonalcoholic Fatty Liver Disease: A Pilot Study. Archives of pediatrics & adolescent medicine. 2009;163(7):674-675. doi:10.1001/archpediatrics.2009.93.

[9] Medina-Navarro R, Durán-Reyes G, Díaz-Flores M, Kumate Rodríguez J, Hicks JJ. Glucose autoxidation produces acrolein from lipid peroxidation in vitro. Clin Chim Acta. 2003; 337(1-2):183-5.. PMID: 14568199

[10] Park YM, Sangeeta R Kashyap SR, Major JA, Silverstein RL. Insulin promotes macrophage foam cell formation: potential implications in diabetes-related atherosclerosis. Laboratory Investigation. 2012; 92, 1171-1780.
doi:10.1038/labinvest.2012.74

[11] Andersen CJ, Blesso CN, Lee J, et al. Egg Consumption Modulates HDL Lipid Composition and Increases the Cholesterol-Accepting Capacity of Serum in Metabolic Syndrome. Lipids. 2013;48(6):10.1007/s11745-013-3780-8. doi:10.1007/s11745-013-3780-8.

[12] Welty FK. How Do Elevated Triglycerides and Low HDL-Cholesterol Affect Inflammation and Atherothrombosis? Current cardiology reports. 2013;15(9):400. doi:10.1007/s11886-013-0400-4.

[13] Bertsch RA, Merchant MA. Study of the Use of Lipid Panels as a Marker of Insulin Resistance to Determine Cardiovascular Risk. The Permanente Journal. 2015;19(4):4-10. doi:10.7812/TPP/14-237.

[14] Sävendahl L, Underwood LE. Fasting increases serum total cholesterol, LDL cholesterol and apolipoprotein B in healthy, nonobese humans. J Nutr. 1999 Nov;129(11):2005-8.

[15] Ende N. Starvation studies with special reference to cholesterol. Am. J. Clin. Nutr. 1962. 11:270-280.

[16] Phinney SD, Tang AB, Waggoner CR, Tezanos-Pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991 Jun;53(6):1404-10.

[17] da Luz PL, Favarato D, Faria-Neto JR Jr, Lemos P, Chagas ACP. High ratio of triglycerides to HDL-cholesterol predicts extensive coronary disease. Clinics. 2008; 64:427-32

[18] Ramsamy TA, Boucher J, Brown RJ et al. HDL regulates the displacement of hepatic lipase from cell surface proteoglycans and the hydrolysis of VLDL triacylglycerol. The Journal of Lipid Research. 2003; 44: 733-741.
http://www.jlr.org/content/44/4/733.long

[19] Chatterjee C, Sparks DL. Hepatic Lipase, High Density Lipoproteins, and Hypertriglyceridemia. The American Journal of Pathology. 2011;178(4):1429-1433. doi:10.1016/j.ajpath.2010.12.050.

[20] Tiainen S, Ahotupa M, Ylinen P, Vasankari T. High density lipoprotein level is negatively associated with the increase of oxidized low density lipoprotein lipids after a fatty meal. Lipids. 2014; 49(12): 1225-32. doi: 10.1007/s11745-014-3963-y. Epub 2014 Oct 31.

[21] Rueda CM, Rodríguez-Perea AL, Moreno-Fernandez M et al. High density lipoproteins selectively promote the survival of human regulatory T cells. J Lipid Res. 2017 Aug;58(8):1514-1523. doi: 10.1194/jlr.M072835. Epub 2017 Apr 4.

[22] da Silvaa JL, Vinagrea CGCM, Morikawa AT et al. Resistance training changes LDL metabolism in normolipidemic subjects: A study with a nanoemulsion mimetic of LDL.
Atherosclerosis. 2011; 219(2): 532-537.
http://www.sciencedirect.com/science/article/pii/S0021915011008185

[23] Mukamal KJ, Clowry CM, Murray MM, et al. Moderate Alcohol Consumption and Chronic Disease: The Case for a Long-Term Trial. Alcohol Clin Exp Res. 2016 Nov;40(11):2283-2291. doi: 10.1111/acer.13231. Epub 2016 Sep 30. Review.

[24] Moderate Alcohol and Cardiovascular Health Trial (MACH15) . https://clinicaltrials.gov/ct2/show/NCT03169530

[25] Leite JO, Fernandez ML. Should we take high-density lipoprotein cholesterol levels at face value? Am J Cardiovasc Drugs. 2010; 10(1):1-3. doi: 10.2165/11319590-000000000-00000.

[26] Zaratin AC, Quintão EC, Sposito AC et al. Smoking prevents the intravascular remodeling of high-density lipoprotein particles: implications for reverse cholesterol transport. Metabolism. 2004 Jul;53(7):858-62.

[27] Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. European Heart Journal,. 2017; 38(32): 2478–2486, https://doi.org/10.1093/eurheartj/ehx163

[28] Devenyi P, Robinson GM, Roncari DA. Alcohol and high-density lipoproteins. Canadian Medical Association Journal. 1980;123(10):981-984.

[29] Volcik K, Ballantyne CM, Pownall HJ, Sharrett AR, Eric Boerwinkle E. Interaction Effects of High-Density Lipoprotein Metabolism Gene Variation and Alcohol Consumption on Coronary Heart Disease Risk: The Atherosclerosis Risk in Communities Study. Journal of Studies on Alcohol and Drugs, 68(4), 485–492 (2007).

[30] Barter PJ, Rye K-A. HDL cholesterol concentration or HDL function: which matters? European Heart Journal. 2017; 0: 1–3
doi:10.1093/eurheartj/ehx274
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[31] Bathum L, Depont Christensen R, Engers Pedersen L, Lyngsie Pedersen P, Larsen J, Nexøe J. Association of lipoprotein levels with mortality in subjects aged 50 + without previous diabetes or cardiovascular disease: A population-based register study. Scandinavian Journal of Primary Health Care. 2013;31(3):172-180. doi:10.3109/02813432.2013.824157.

[32] Mente A, Dehghan M, Rangarajan S et al. Association of dietary nutrients with blood lipids and blood pressure in 18 countries: a cross-sectional analysis from the PURE study.
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PURE lipids and BP

What is The Ketogenic Diet?

Your diet is perhaps the most important factor controlling your health and well-being. Sure, other factors do play a role, but diet is the linchpin of the incredibly complex human biology. So, if you are trying to get rid of those love handles or get back in shape, a good diet can take your efforts to the next level.

But the question is:

What is the best diet for weight loss?

Well, as it turns out, a ketogenic diet (or keto diet) is one of the most effective nutritional strategies to lose weight and improve overall health. Multiple scientific studies have backed up this notion time and again. Consequently, it is rapidly taking over the health and fitness world and millions of people swear by it.

If you are new to the whole ‘keto’ thing, you may have millions of questions swirling in your head. But finding definitive, unbiased and easy to understand answers to them can be difficult.

Well, that’s where we come in. In this article, we are going to answer all the questions you may have about keto diet and then some. And while we are at it, we are also going to learn some cool and exciting facts about your body as well. So, let’s get going!

What is a Ketogenic Diet?

It is an obvious question that needs to be answered before anything else. In a nutshell, a ketogenic diet is a diet that is very low in carbohydrates.

You see, any food you eat contains three major nutrients that provide you the bulk of the energy (or calories) that you need. These three major nutrients (also called macronutrients) are:

  • Carbohydrates

  • Proteins, and

  • Fats

Anything that you eat will contain all of these three macronutrients in varying proportions. A typical diet usually contains a higher proportion of carbohydrates and lower proportions of proteins or fats. A ketogenic diet, on the other hand, limits the number of carbohydrates to a minimum.

Traditionally, a keto diet allows you to eat 20-30 grams of carbs each day. The exact proportion of carbs, fats, and proteins will vary depending on your current health status and what you want to achieve.

That said, a standard keto diet has 70-80% of the daily calories supplied by fats, 15-20% provided by proteins and the rest by carbs; which is around 5%.

Compared to other ‘low-carb’ diets, a keto diet does not overload your body with proteins, and there is a good reason for that. When you limit the intake of carbs in your diet, proteins can be converted to glucose in your body via the process known as gluconeogenesis. If this happens in considerable amounts, the whole point of a low-carb diet is moot! Hence, a keto diet relies on fats to give you most of the energy you need.

A brief history of ketogenic diet

The basis of beneficial effects of cutting down carbohydrates in the diet originated in a study conducted by researchers at the John Hopkins University in the 1920s. When researchers at the prestigious University were studying the effect of fasting on patients who had epilepsy, they found that it had a positive effect on their body fat as well.

However, fasting for extended periods of time is not feasible. Therefore, scientists developed the next best thing: a diet that mimics the effects of fasting. They found that when you cut down carbs in the diet, the body can be ‘tricked’ into believing that you are fasting and the keto diet was born! We will return to the topic of how exactly a ketogenic diet works in the following sections.

What are The Benefits of a Keto Diet?

The obvious advantage of a keto diet is that your body starts burning the stored fat and you can lose weight quickly. However, a keto diet has many other long-term benefits as well. Many studies conducted with low carbohydrate diets have indicated plenty of health benefits that go beyond just weight loss.

Here are some of the most significant health benefits of a keto diet.

1. Greater and more importantly, faster weight loss

One of the most noticeable benefits of a keto diet is faster weight loss, especially during the first few weeks of the diet.

Many studies have shown that people who limit the intake of carbs in their diets tend to lose more weightfaster compared to individuals who reduce fat intake.

The rapid weight loss on a keto diet can be understood if you take a look at what happens to your body on a keto diet. When you restrict the intake of carbs, your body gets rid of a lot of unwanted water. As the insulin levels drop following a keto diet, your kidney gets rid of more sodium and with it a lot of unnecessary water.

The combined effect is that you feel less bloated and lose weight rapidly for the first few weeks.

The best part of a keto diet is that you lose a ton of more weight, often 2-3 times more compared to a low-fat diet, without having to starve yourself. A great benefit of ketosis!

In my books, that’s a win-win move right there!

2. You get rid of the fat from the ‘worst’ parts

Here is a question for you:

If you can choose, from where on your body, do you want the fat to disappear?

I bet most of you said the abdomen, hips or the belly, right?

Well, as it turns out, a ketogenic diet gets rid of the fat from the abdomen and belly area much more efficiently than any other non-surgical procedure.

Apart from the aesthetics, the abdominal fat is also very harmful to your health. You see, when the fat accumulates in the abdomen, it increases the risk for cardiovascular diseases including heart attacks,strokes and diabetes.

If you follow a ketogenic diet for a longer period, you will see a decline in the abdominal fat and the various health risks associated with it.

3. Improvement in your lipid profile

Fat is essential for the proper functioning of your body. It is an essential nutrient that is indispensable for various body process. However, fat is not a just one substance; it is a category of molecules.

Several molecules make up the ‘fat’ of your body. The proportion of these molecules is as important as the amounts.

For instance, cholesterol is a fat molecule that is essential for the proper functioning of the brain and healthy skin. However, it comes in several ‘types, ‘ and not all of them are good. Actually, the proportion of the ‘good’ cholesterol (HDL) vs. the ‘bad’ cholesterol (LDL) is much more important than the total cholesterol you have.

A keto diet not only gets rid of the excess fat but also restores the healthy balance between various types of fats in the body.

For instance, a low-carb keto diet has been shown to increase the proportion of healthy HDL cholesterol and decrease the unhealthy LDL cholesterol in your body.

There have also been studies showing that a keto diet can lower the proportion of other fat molecules called triglycerides that are bad for you.

4. Reduction in blood glucose level

The carbs that we eat are eventually converted into glucose by the body. If your diet contains a lot of carbs, you tend to generate a lot of glucose in your blood, which is not a good thing.

The elevated levels of glucose in the blood are harmful, and the body releases a hormone called insulin to mitigate this situation. Under the influence of insulin, the cells of the body absorb this glucose from the blood.

The insulin system works for most people, but for people with diabetes, it fails miserably. People with diabetes produce fewer quantities of insulin, and any ‘spike’ in blood glucose levels can have a toxic effect on their bodies.

A keto diet attacks this problem at its roots. By consuming fewer carbs, the risk of generating that dreadful glucose spike in diabetic patients can be completely avoided.

Some studies have shown the positive effect of a keto diet on lowering blood glucose levels in diabetic patients.

5. Can help you reduce blood pressure

High blood pressure or hypertension is one of the biggest health risks around the world. As a matter of fact, one in every three people in the United States has high blood pressure. It is estimated that almost 1000 people die due to hypertension related issues every single day.

A ketogenic diet can be very effective in controlling hypertension according to multiple studies. Consuming fewer carbs in the diet decreases the blood pressure in hypertensive and pre-hypertensive individuals resulting in a reduction in risks of diseases such as stroke, kidney failure, and cardiac arrest.

6. Can suppress appetite

One of the biggest hurdles in staying on a diet has to be the hunger. I mean if you have tried to go on any diet program, you know what I am talking about. You are hungry all the time!

The great thing about a ketogenic diet is that it can gradually decrease your appetite over time. Multiple studies have shown that a diet that is high in fats and proteins compared to carbs can reduce your appetite. You won’t feel the craving for junk food on a ketogenic diet.

The bottom line is:

A ketogenic diet can healthily reduce your appetite, and you can stick to the diet for a longer time. You won’t feel bouts of hunger that you might feel with almost any other diet.

7. Good for certain neurological issues

A ketogenic diet can be quite an effective strategy to manage certain neurological issues including epilepsy. As a matter of fact, the roots of a ketogenic diet can be traced back to the epilepsy study that we discussed earlier.

There has been extensive work on the effects of a ketogenic diet on children with epilepsy, and most studies have found a positive correlation. Many children who are not responsive to drugs often show marked improvements with a ketogenic diet.

Devil’s Advocate

So, there is a ton of evidence about the benefits of the ketogenic diet, but it has its fair share of controversies as well. Many people believe that the risks associated with a strict ketogenic diet should not be overlooked for the sake of dropping a few extra pounds.

Some of the most common criticisms regarding the ketogenic diet include the following.

Ketosis in a long term may cause muscle loss

While most experts agree that a ketogenic diet that forces the body to undergo ketosis is effective initially, some of them are skeptical regarding the long-term benefits.

Some dieticians believe that entering a prolonged ketosis can do more harm than good to your body. They think that a prolonged state of ketosis can cause muscle degeneration. The keto-skeptics have argued that this diet is not ideal for people who want to reduce fat but gain muscle.

However, many scientific studies have debunked this as a myth. According to some papers, a keto diet can actually preserve muscle loss rather than accelerate it.

It is not possible to carry on the good initial results

When your body enters ketosis, you see a rapid weight loss in the first few weeks. It is due to the metabolic shift that is happening in your body and mainly through the loss of a lot of unwanted water. However, as you progress in the diet, it can get harder to replicate the initial success.

Many people wrongly think that they will continue the same rate of weight loss as they observed during the initial phase of ketosis. The fact of the matter is the initial weight loss can be rapid, but it will taper off eventually. After losing a considerable amount of weight, you will experience a drop in the rate of weight loss, but if you carry on, you will see your weight dropping steadily.

Ketosis is a short-term solution

Many skeptics of the ketogenic approach believe that when you are on a ketogenic diet, you are essentially starving yourself. As a result, they believe that weight loss is natural. But as soon as you stop the diet, which according to them is inevitable, you will gain the weight right back.

Now, there might be some truth to this argument. As a ketogenic diet is stringent, there may be a problem for some people to stick with it for a longer term. However, a ketogenic diet is not a fad or a temporary thing that you try. It is a lifestyle choice that you make to get healthy. It can help you shed that extra weight and motivate you to carry on.

The truth is:

Despite numerous scientific studies, the ketogenic diet has repeatedly been found to be efficient and safe.

That said, if you become obsessed with your weight, it is never a good thing. The problem is not the diet per-se, but the misguided approach that some people take with the ketogenic diet.

What are Carbohydrates and Their Role in The Body?

As we saw earlier, a ketogenic diet limits the amount of carbohydrates that you can consume. But, what are these carbohydrates and what do they do in your body?

Chemically speaking, all carbohydrates are molecules that contain three elements- carbon, hydrogen, and oxygen.

These are often called energy molecules as the body can generate energy by metabolizing them in the cells.

Carbohydrates can range from simple carbohydrates such as glucose or fructose to highly complex carbohydrates such as starch and glycogen. Carbohydrates are sometimes also referred to as ‘saccharides’ as most of them have a varying intensity of sweet taste. Depending on their chemical structure, carbohydrates are classified into the following categories.

Monosaccharides

These are the simplest forms of carbs and contain a single molecule in their structure. Some of the most common examples include glucose, galactose, and fructose. Of all the monosaccharides, your body can use only glucose as a fuel.

So, when we are talking about blood sugar, we speak of glucose, which is a monosaccharide.

Disaccharides

As you can probably guess from the name, Disaccharides contain two monosaccharide molecules linked together by a chemical bond. Examples of disaccharides include sucrose or table sugar that contains one glucose and one fructose molecule. Lactose is another disaccharide that contains one glucose and one galactose molecule.

Polysaccharides

If you join multiple monosaccharide molecules together in chains, you end up with a large molecule called a polysaccharide. Sometimes, these chains are unbranched and linear such as in starch, or sometimes they are branched as in glycogen.

As you can imagine, almost everything that you eat contains carbohydrates. Anything that contains starch or sugar contains carbohydrates.

However, to be used by the body, a carbohydrate needs to be converted into glucose within the body. That said, some carbs are easily converted into glucose while others are not. For instance, table sugar, or sucrose, is easily and efficiently converted into glucose. As a matter of fact, the process is so fast that as soon as you eat a sugary dessert, your blood glucose level shoots up!

Starches are also easy to break down to glucose and result in high concentration of glucose in the blood after ingestion.

The capacity of a food item to cause an increase in the concentration of glucose in the blood is called the Glycemic Index (GI). The higher the GI of a food item, the bigger spike in glucose level it causes after you eat it.

Fruits, potatoes, milk products, all have a high GI. Hence, these foods can significantly increase your blood glucose levels.

But, from what we have seen about carbs till now, they seem to be quite good for you, right? So, why shun them?

Are carbs bad?

Well, carbs are not bad at all. In fact, they are the fuel that drives your body. However, if you overeat the wrong carbs, and you always do, you can trigger a rather unpleasant chain of events.

Let me explain:

You see, it all boils down to the insulin-glucagon hormonal system. When you are fasting, and your body needs glucose, the alpha cells of your pancreas secrete a hormone called Glucagon. It stimulates the liver to release some stored glycogen that in turn is converted into glucose and your blood glucose level rises.

In response to this elevated blood glucose level, the beta cells of the pancreas release a hormone called Insulin. It, in turn, stimulates the cells of your body to take up glucose and use it to generate energy.

Now, imagine if you are eating a lot of high GI carbs, day in and day out. Your blood glucose levels are always high. There is no need for the generation of glucagon from the alpha cells, and glycogen never gets used up.

There is a stress on the beta cells of the pancreas to clear up the excess glucose from your blood. So, they secrete more insulin. Now, over time, the higher levels of insulin in the blood cause the cells of your body to acquire a form of resistance to insulin, and they need more insulin to get stimulated to clear up the elevated glucose from the blood. Soon, there comes a time when even a high concentration of insulin is not enough to cause the cells of your body to take up glucose from the blood.

The overall result is that your blood glucose levels shoot up and right there lies the root of all health problems.

The elevated glucose levels can cause hypertension, obesity and a host of other health concerns. Not to mention, when under constant stress, your pancreas gives up, and the problem is amplified.

So, what is the solution?

Well, the solution is to limit your intake of high GI carbs in the first place. The ketogenic diet is based on this very principle. By restricting the amount of high GI carbs to a minimum, you can avoid the glucose spike in your blood and the whole cascade of events.

If you have a lot of fat stored in your body, the body will soon start using this fat to generate energy, and you will start losing weight.

Ketogenic Food List

So, you need to limit the intake of carbs in your diet. But as you just saw, almost anything and everything has carbs in it, right? Well, not really.

As it turns out, there are many healthy alternatives to carbs that will provide you with all the energy you need without spiking your insulin and blood glucose levels.

Remember, a ketogenic diet requires you to replace the calories coming from carbs with the calories coming from proteins and healthy fats. So, there are a ton of options for you, don’t worry!

Here is a ketogenic food list that you can include in your keto diet. You can eat the following high fat, low carb foods freely

Protein

You can consume good quality meats and other plant-based proteins to cover for carbs. Some of the best options include:

  • Grass-fed meats such as beef, lamb, goat or even venison

  • Poultry such as chicken, turkey, duck, and goose

  • Cage-free eggs

  • Fishes such as tuna, bass, sardines, salmon and mackerel

As a word of caution, try to include lean meats in your diet as much as possible. Red meats such as beef and pork are also high in cholesterol. Make sure you change up your proteins with lean chicken breast or fish occasionally.

Healthy fats

Contrary to popular belief, fats are not bad for you at all. As a matter of fact, fats are essential for the proper functioning of your nervous system. However, avoid saturated fat as much as possible. Go for polyunsaturated fats, and you should be okay. Here are some of the fats that you can eat on a keto diet:

  • Avocado oil

  • Cold pressed coconut oil

  • Polyunsaturated fats

  • Olive oil

  • Linseed (flax) oil

  • Lard

  • Butter

  • Ghee

Ketogenic Vegetables

Veggies are rich in many micronutrients such vitamins and minerals. You can eat as many veggies you like on a keto diet. The only catch is that they should not be starchy. So, a potato is a strict no, but spinach is a yes!

Here are some ketogenic vegetables that you can eat on a keto diet:

  • Any leafy greens. These include spinach, collard greens, kale, mustard greens, lettuce.

  • Cruciferous veggies such as broccoli, cabbage, brussels sprouts and cauliflower

  • Fresh herbs such as cilantro, rosemary, thyme, mint and a lot more

  • Zucchini, leek, celery, chives, and cucumbers

  • Some slightly high carbs containing veggies such as asparagus, mushrooms, bean sprouts, bell peppers, sugar snap peas, wax beans, and tomatoes

You also have a good selection when it comes to snacks as well. Some of the foods that you can eat as snacks while on a keto diet include the following:

  • Beef or turkey jerky

  • Veggies with homemade dressing

  • Boiled eggs

  • Minced meat

Evan some condiments are also permissible on a keto diet. The list includes:

  • Apple cider vinegar

  • Herbs and spices

  • Unsweetened mustards and unsweetened hot sauce

If you are a fan of hot beverages, you can add tea, and coffee without milk or sugar (in moderation) or bone broth.

You can also eat the following moderately high carbs containing foods occasionally, but limit the intake

  • Dairy products (full fat)

Limit intake of dairy products as they contain sugars and carbs. But if you want to indulge occasionally, make sure you are consuming high fat-containing dairy products. Such items include:

  • Full-fat cow’s milk
  • Hard cheeses
  • Medium starchy veggies

  • Parsnips
  • Sweet pea
  • Okra
  • Carrots
  • Beets
  • Potatoes
  • Yams
  • Legumes

  • Chickpeas
  • Kidney beans
  • Lentils
  • Hummus
  • Nuts and seeds

  • Almonds
  • Walnuts
  • Cashews
  • Chia and flax seeds

Foods to completely avoid

If you are on a keto diet, certain foods are completely off limits. Some of the prominent ones include sugars, syrups, and bread. Here are some foods you can think of as a “anti-ketogenic food list”:

  • All grains

All grains contain a ton of starch, and hence they are completely off limits on a keto diet. Grains include the supposedly healthy grains as well including the following:

  • Rice
  • Quinoa
  • Wheat and any form of bread
  • Corn and corn products
  • All processed foods

Processed food contains a ton of sugar, and hence they are not allowed on a keto diet. Some of the processed foods that are entirely banished include:

  • Chips
  • Sweets
  • Cakes
  • Cereal
  • Oatmeal
  • Chocolates
  • Canned foods including soups
  • Foods with artificial sweeteners
Fatty foods

Alcohol on a Ketogenic Diet

alcohol in diet

One of the more common questions about a keto diet is whether alcohol and ketosis mix.

The answer to this question is not as straightforward as you may think. Your body can use alcohol as a fuel to generate energy; just like it uses glucose.

Hence, when you consume alcohol during a ketogenic diet, assuming you picked a low carb beverage, your body burns off the alcohol instead of the fat.

Now, the impact of this phenomenon on your weight loss can vary depending on the individual.

I know some people who have little effect of consuming small amounts of alcohol occasionally on their weight loss. However, I also know a few individuals who experience a complete halt in their weight loss as soon as they consume alcohol.

So, there is not a simple answer to the question.

Should I completely avoid alcohol?

Well, as I pointed out, the impact of alcohol on weight loss varies from one individual to the other. So, it is not possible to say unequivocally that you should ban alcohol from your diet.

The best foot forward will be to try a moderate amount of alcohol and see how it affects your body. That way, you can make an educated guess regarding the inclusion or exclusion.

How will my ketogenic diet impact my buzz?

I thought you would never ask! Just kidding!

The thing is, your alcohol tolerance goes down on a keto diet. So, you will get drunk fast! There are a couple of reasons for this. First, your body will be metabolizing alcohol almost immediately. What this will do, is get you drunk quickly. Secondly, you will not be eating a ton of carbs that can help you to soak up the alcohol and slow down the process of intoxication. As a result, all the alcohol you drink is readily available for absorption, and you get tipsy quicker. Alcohol and ketosis can be a dangerous mix if you aren’t careful.

Whether you decide to indulge in an occasional alcoholic drink, make sure that you are sticking to the low carb variety. Some of the beverages that you can try includethe following:

  • Hard liquors such as whiskey, brandy, tequila, vodka, rum, gin, and scotch

  • Low carb beers

  • Low carb wines such as Merlot (3.2g of carbs), Pino Noir (3.4g of carbs), Champagne/Sparkling Wine (1.5g of carbs)

What is Ketosis?

The ketogenic diet is an excellent way to get your weight down and get back in shape. Over the years, this approach has been refined, validated and used by millions to get rid of their body fat safely and efficiently.

But what does a keto diet do to your body?

Well, to answer these questions, we will have to dig just a little deeper into the physiology of the human body. Don’t worry; I am going to keep it as easy to understand as I can!

So, to figure out what is the effect of the keto diet on your body, let’s see what the term ‘keto’ means. It is a short form of the word ‘ketosis.’ It is a healthy state of your body when most of the energy is not coming through burning glucose, but through burning what are called ‘ketone bodies.’

What are Ketones?

Ketones or Ketone bodies are fuel molecules just like glucose that the cells of your body can use to generate energy. But the most interesting thing about them is that they are produced by burning the stored fat in your body.

You see, when you are fasting, there is no supply of glucose from the diet to use. But your body, especially your brain, needs a lot of energy to function. So, there is a mechanism in place to convert the stored fat in the body to ketone bodies that can be used to generate energy. It is the reason why your body stores fat in the first place!

When you consume a diet that is very low in carbohydrates and moderate in proteins a.k.a a ketogenic diet, the body assumes that you are fasting and initiates the ketosis process. It is called metabolic ketosis as your body is burning off fat due to the lack of glucose in your blood.

However, metabolic ketosis should not be confused with diabetic ketosis. In the case of a diabetic ketosis, there is a lot of glucose in the blood, but due to insulin resistance, the body can’t use the glucose and relies on burning ketone bodies instead. This type of ketosis is horrible for your body. It can create a ton of problems and is one of the worst nightmares in managing diabetes.

How do You Enter The State of Ketosis?

Ketogenic Diet Tips

Your body enters a state of ketosis if you fast for about 3-4 days. It forces the body to rely on ketone bodies for energy, and it makes them by burning the stored fat.

Many so-called tips and tricks promise a faster way to enter the state of ketosis. However, the best way to achieve ketosis is through proper diet. There is no short cut or a gimmick that can take you there.

You can enter ketosis if you follow the following guidelines:

  • Restrict the intake of carbs to less than 20g a day.

  • Limit your protein intake as well. As we discussed earlier, proteins can be converted into glucose when you restrict carbs in your diet. If you don’t limit the amount of proteins in your diet, it will be challenging to enter into a ketosis phase.

  • Forget about counting your fat intake. You are not going to lose weight on a keto diet if you are starving yourself. A bulk of the calories in a keto diet need to come from fat. So, stop worrying about eating fats.

  • Drink plenty of water. Make sure that you are drinking at least one gallon of water a day on a keto diet. It will help you to stay hydrated as well as curb hunger.

  • Start working out. Exercise is a great way to boost your metabolism and a good way to enter ketosis.

How do You Know If You are in Ketosis?

So, you are doing everything right. You have limited your carb intake as well. But how do you tell whether you have entered the coveted ketosis phase?

Well, it is not that difficult to tell if you are in ketosis. The best and most definitive way to answering this question is using blood or a urine test strip. You can use these strips at home, and they can tell you whether you have entered ketosis or not.

While the urine strips are less accurate compared to the blood strips, they are less costly as well.

If you are not interested in testing your urine or blood, there is an alternative way as well. Many signs can indicate that your body is in a state of ketosis. These signs will tell you whether you are on the right track or not.

ketone body testing kit

Container with urine and test-strips for the analysis. These can be used to test for a state of ketosis

If you need to go to the bathroom more often

If you have just started a keto diet; increased urination frequency is a good indicator. Ketosis causes diuresis or increased urination. So, if your bathroom visits have markedly increased, pat yourself on the back, you are heading in the right direction.

If your mouth is dry

A dry mouth is yet another hallmark of ketosis. If your body enters ketosis, you urinate frequently and lose water. As a result, your mouth feels dry. Make sure that you are drinking plenty of water during a keto diet to stay hydrated.

If your breath is bad

One of the main ketone bodies that your body is generating when it is in ketosis is Acetone. It is a volatile liquid that can be exhaled by lungs. There is only one drawback of this. Acetone has a bad smell to it. It smells like over ripe fruit or a nail polish remover. If you experience a bad breath during a keto diet, it is probably due to the acetone. Don’t worry, though; it will go away in the long term.

If you don’t feel hungry but yet quite energetic

Another hallmark of reaching a keto state is reduced hunger and a clear mind. You will start to feel more energetic and lose all the cravings for those mid-day or late-night snacks.

What to Expect on a Keto Diet?

A ketogenic diet is one of the best ways to lose weight, but it can be a bit overwhelming in the beginning. However, if you know what to expect when you are on a ketogenic diet, managing the temporary side effects can be easier.

When your body enters ketosis, it is undergoing a significant change in the most fundamental way possible. It is only natural for the body to reach to this change that you are imposing on it before it gets used to it.

There are certain ways in which your body is going to respond to your ketogenic diet. Some of these ways can have quite an unpleasant effect as well.

However, there is good news:

These effects are only transitional. Once your body adapts the “keto way” you will see these effects fade away and you will have more energy than ever before.

In the meanwhile, you can see some so-called side effects of a ketogenic diet. Let’s see what they are.

1. The keto flu

One of the most prominent reactions to a keto diet is the keto flu. But what is the keto flu? The symptoms of keto flu are just like the regular flu. You will experience tiredness, dizziness and overall lack of energy. Most people experience extreme fatigue during this phase of the ketosis.

You may even feel some lack of mental focus as well during this phase of ketosis.

Although you will want it to end, it is going to take its time to get over. In the meantime, you must stay determined and keep going strong.

Most people experience the worst symptoms in the first week of ditching the carbs. However, in some people, the symptoms can last for up to 5 weeks as well.

How to manage keto flu symptoms?

If you are experiencing the symptoms of keto flu, you can take steps to make it more bearable. Here are some tips that will help you get through this tough phase.

  • Eat more fats: Starving yourself is the worst thing you can do on a keto diet. If you suddenly stop eating carbs, your body will feel the pinch in the worst possible way. It still needs the energy to function, and you must provide it; in the form of fats. So, eat plenty of fats such as butter, ghee, and lard. As soon as you put more fat calories in your body, you will start feeling better.

  • Drink plenty of water: When your body enters ketosis, you lose a lot of water. If you don’t replenish the lost water, you can leave your body dehydrated, and it can worsen the symptoms of keto flu. Make sure you are drinking at least a gallon of water when you start a keto diet.

  • Add more salt to your diet: Your body loses a lot of sodium when it enters ketosis. Replacing the lost sodium is essential for the proper functioning of the body. So, you should add more salt to your diet to replenish the lost sodium.

  • Eat a few moderate carbs if you must: Going on a strict keto diet can send your body into a state of shock. If you crave for carbs, adding a few foods that have moderate amounts of carbs is not such a bad idea. Just make sure that you are not overdoing it. Remember, if you feel crappy, you are not likely to comply with the diet anyway. So, it is better to bea bit moderate in the beginning if it means a better long-term compliance.

2. Loss of physical strength

During the initial phases of the keto diet, it is quite common to experience a lack of physical strength. If you lift weights, you will feel that suddenly, your strength is not there. It is quite a natural reaction of your body to a keto diet.

Make sure you are drinking plenty of water, replenishing your electrolytes and most importantly, not starving yourself. Soon, you should feel good again, and as soon as this initial phase blows over, you well get back the energy you once had and then some! So, stick it out my friend, for there is something great to come!

The bottom line is:

During the initial phase of ketosis, you are going to feel, well, crappy! That’s the truth. But always remember that all these effects are transient, and they will go away. Soon, you will see your fat melting away and your energy levels better than ever.

So, stick it out and make sure you are following the tips mentioned above to make this initial phase as bearable as you can.

Famous People Who Like Keto

The effectiveness of a keto diet has turned many famous people into die hard keto fans. From movie stars to professional athletes, everyone seems to sing high praise of this amazing diet.

Some of the most beautiful women in the entertainment industry swear by the keto diet. Megan Fox, Adriana Lima, and even Kim Kardashian follow a ketogenic diet to stay in shape and keep up the energy for their busy schedule.

Some of the most successful professional athletes also follow a keto diet. LeBron James and Kobe Bryant are among the many pro basketball players who found that low-carb, high-fat diet helped them add that extra oomph to their game.

The point of mentioning all these celebrities is this:

The keto diet works! Just imagine, all these famous people have all the resources at their disposal. They have the best experts advising them. If they think that something works, theremust be some truth to it, wouldn’t you think?

Again, I am not saying that you should start a keto diet just because LeBron James is on it or Megan Fox is on it, but the fact that they are is kind of a big deal! Don’t you agree?

Besides, there is a ton of scientific evidence that supports the keto diet. So, it does not need any celebrity endorsements in the first place!

Something to Take Home

People who are trying to lose weight and get back in shape often don’t realize the impact a good diet has on their efforts. While they are ready to immerse themselves into all kinds of exercise routines, they pay little attention to their diet. As several research papers have pointed out, exercise or health supplements alone just don’t work if they are not complemented with a good diet. And a keto diet has the potential to transform your body like never before.

So, there you have it, this is everything, well almost everything, that you need to know about the ketogenic diet! It is quite a smart strategy if you think about it, isn’t it? Once your body transforms from a ‘fat-conserving mode’ to a ‘fat burning mode,’ dropping those pounds is not that difficult!

Don’t believe the LIES about Garcinia Cambogia

pinocchio_lying
Since the late 1990’s Garcinia Cambogia has been included in various weight loss products, but exploded in popularity in 2012 when Dr Julie Chen talked about it on the Dr Oz TV show.

Unfortunately, there is an avalanche of faulty information about Garcinia Cambogia on the web that we attempt to clean up below.

WHAT THE RESEARCH SAYS

photo-research-woman-in-lab

Several studies on rats have demonstrated significant weight loss, belly fat reduction, and lowered blood glucose levels (456).

We looked at all the randomized, double-blind clinical studies on humans. Some we excluded were either too short (2 weeks), used too small a dose, or had other flaws such as a low fat, high carb diet which researchers believe had a negative impact on the results.


This chart shows the results from the most relevant clinical studies on Garcinia Cambogia, encompassing 307 participants (7,8,9,10).

All of these were Double Blind,Randomized Controlled Trials, with subjects given Garcinia Cambogia or Placebo over 8-12 weeks.

The average for these 4 studies was 4.1 pounds lost vs 1.7 for those taking Placebo.

It should be noted that studies #3 and 4 used the highest dosages of 2800 mg daily, and showed the greatest amount of weight loss compared to placebo.

Studies #1 and 2 showed the least amount of weight loss benefit, and also used the lowest amount of Garcinia Cambogia, at 1200 mg per day.

[box]Conclusion: The average for the 4 relevant clinical studies on humans showed weight loss of 3 pounds more than placebo. Studies that used higher doses of HCA recorded more weight loss. [/box]

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What brand of Garcinia Cambogia should you Buy

You really need to read the label. Many brands are pushing inferior products. If they don’t show you the label, chances are they are trying to push you some crappy, useless stuff and don’t want you to realize it until you take it and don’t get any results.

Always Look for the HCA!

HCA, or hydroxycitric acid, is the active ingredient. You need to make sure it has at LEAST 60% HCA in it – Higher is better. Also check to make sure they don’t use a lot of added ingredients – especially if they’re hard to read, nearly impossible to pronounce ingredients.
wwrecommend
We’ve looked at all the leading brands sold on Amazon. There are several that are good, and dozens that are garbage.
The best quality we found that also has a good price is NewLifeBotanical’s Garcinia Cambogia.
If you find it more convenient, you can get it on Amazon

[product_category category=”garcinia-cambogia-2″ columns=”3″ per_page=”6″ orderby=”menu_id” order=”desc”]

Reasons why we recommend it:

  • Has 90% HCA!
  • No filler ingredients – all natural only
  • 600mg per capsule
  • Has been PROVEN to be effective
  • Has NO additives, fillers and other low-quality ingredients

 

PHARMACEUTICAL COMPANIES HATE GARCINIA CAMBOGIA

According to this article in Washington Post, it cost between $800 million and $2.6 BILLION to bring a new prescription drug to market.

Once they start clinical trials, the pharmaceutical company only has 20 years of patent protection to recoup that cost, so they have to charge exorbitant prices to make that back and pay their shareholders a good return on their investment.

Of course they don’t want potential customers to think a natural product that cost a tiny fraction of what they charge can be effective at all.

Hence pharmaceutical manufacturers often fund research studies they hope will cast the competition in a bad light. A few million dollars to fund a study on a competitor is nothing compared to the billions it cost to develop a drug.

For example, this meta-review that examines existing clinical studies on Garcinia Cambogia is funded by GlaxoSmithKline, the manufacturer of the prescription weight loss pill Orlistat, marketed under the name Alli.

For reference, Alli cost $60 for 120 capsules! The literature claims it can block 25% of the fat you eat from being absorbed.

Not surprisingly, the research they pay for often finds mixed results, with some studies showing positive effects for Garcinia Cambogia and some not.

The academic editor for that meta review was also the lead author for a few of the studies that found Garcinia to be ineffective. He also was the lead author for several studies that showed positive results for Orlistat (1,2,3).

[box] Conclusion: Big Pharma spends hundreds of millions of $$$ funding research to cast doubt on the effectiveness of natural weight loss products like Garcinia Cambogia.
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HOW DOES IT HELP WITH WEIGHT LOSS?

Garcinia Cambogia is somewhat unique in that there are 2 pathways the HCA utilizes to help with weight loss

1. It May Help Reduce Hunger

too hungry

Studies with rats have shown those given Garcinia Cambogia tend to eat less than those in the control group(11, 12).

How it works isn’t fully known, but those studies seem to indicate it increases levels of serotonin in the brain. (13, 14).

Likewise, some clinical studies with humans has shown it tends promote feeling of satiety (fullness), so you eat less. (15, 16, 17, 18, 19).

Serotonin is the “feel good” hormone that promotes feelings of satisfaction and is well known to be an appetite suppressant. (20).

Those studies are in contrast to some others that found no benefit for suppressing appetite vs those given placebo. (21, 22, 23, 24). Its not clear why studies have shown such a difference and more study is needed.

Conclusion: Some studies have shown garcinia cambogia increases serotonin to suppress appetite, but there have been other studies that could not replicate this effect.

2. It May Block Fat Production and Reduce Belly Fat

The effect HCA has on fatty acids in the bloodstream is the most important factor in its ability to aid weight loss.

Human and animal studies has shown HCA helps lower levels of triglycerides in the blood, reducing the oxidative stress throughout the body. (25, 26, 27, 28, 28).

It is even more attractive as a weight loss aid as it helps reduce belly. (29).

Another study gave moderately obese individuals 2,800 mg of garcinia cambogia daily for eight weeks (30).
After completion, participants had dramatically lower markers of metabolic disease such as:

  • 6.3% LOWER Total cholesterol levels
  • 12.3% LOWER LDL (the “bad”) cholesterol levels
  • 10.7% HIGHER HDL (the “good”) cholesterol levels
  • 8.6% LOWER Blood triglycerides

This is due to the inhibition of the enzyme citrate lyase, which signals the production of fat in the body (32, 33, 34, 35, 36).

By inhibiting citrate lyase, garcinia cambogia is thought to slow down or block fat production in the body. This may reduce blood fats and lower the risk of weight gain, two major disease risk factors (37).

Conclusion: Garcinia cambogia blocks the production of new fats in the body, and has been shown to lower cholesterol levels and blood triglycerides in overweight people.

OTHER HEALTH BENEFITS

Animal and test-tube studies suggest that garcinia cambogia may also have some anti-diabetic effects, including (38, 39, 40):

  • Decreasing insulin levels
  • Decreasing leptin levels
  • Reducing inflammation
  • Improving blood sugar control
  • Increasing insulin sensitivity

Garcinia cambogia may also have benefits for the digestive system. Animal studies have suggested it helps protect against stomach ulcers and reduce damage to the inner lining of the digestive tract (41, 42).

However, these effects need to be studied further before firm conclusions can be drawn.

Conclusion:Garcinia Cambogia may help lower blood sugar levels and increase insulin sensitivity to combat diabetes

 

SIDE EFFECTS

Generally Recognized as Safe (GRAS)
thumbs up

Garcinia Cambogia is recognized as GRAS by the FDA, meaning it has “been adequately shown to be safe under the conditions of its intended use”.

There have been several studies to test the effectiveness of these products and in these controlled quantities there were no significant side effects.

This meta-analysis examined all published research on Garcinia Cambogia, and found garcinia to be free from any major side effects when taken at dosages up to 2800 mgs per day (with 60% HCA)

Screenshot 2016-03-28 12.30.09

WHO SHOULD NOT TAKE GARCINIA CAMBOGIA

garcinia warning

It  IS safe for most people. But there are a few cases where you wouldn’t want to take it:

  • Pregnant
  • Breastfeeding
  • Alzheimers or dementia

Garcinia Cambogia boosts serotonin levels in the brain (which triggers the satisfied, full feeling that helps suppress appetite).

For this reason, it is not advised for patients with neurological disorders such as Alzheimers, Parkinsons, or other forms of dementia.

DOSAGE AND WHEN TO TAKE IT

Dr Harry Preuss is  a researcher and pathologist at Georgetown University past president of the American College of Nutrition who has led 2 of the studies on HCA that showed the best results (43,44)  He says:

“YOU HAVE TO TAKE THE RIGHT DOSE OF THE RIGHT PRODUCT, AND YOU HAVE TO TAKE IT PROPERLY.”

The 4 studies that were included in the meta-analysis referenced above noted that 1 to 2.8 grams daily were used in testing, and that 2.8 grams seemed more effective (45)

Different studies that have been performed to focus on side effects found no major side effects at dosages up to 2.8 grams daily (46).

Dosage recommendations from those studies are:

  • 500 to 1000mg capsules
  • 70% or higher HCA
  • 3 times a day
  • 30-60 minutes before meals
  • taken with 8 ounces of water

70% HCA means that the manufacturer has standardized the extract to be 70% Hydroxycitric Acid by volume.

50-60% was the highest purity commercially available until recently, so has been the standard used for testing.

The higher percentage provides more total HCA per capsule, but is not more effective otherwise.

In other words, the higher HCA % is not “better”,  you just need less of it.

For proper dosage, you should lower the quantity if you use a product with HCA % higher than the 60% used in studies.

For example, the maximum recommended dosage of 3 grams per day of a 60% HCA product would yield 1800 mg of pure HCA – the same as 2 grams of 90% HCA.

[box]**** DAILY MAXIMUM RECOMMENDED DOSAGE ****

3,000 mg  x 60% HCA =   1800mg  pure HCA
2,000 mg  x 90% HCA = 1800mg  pure HCA[/box]

BUYING ON AMAZON – BEWARE THE SCAMS

here_today_gone_tomorrow
With any popular diet product, there are lots of scams that sell crappy product at ridiculous prices, and some that disappear with your money.

You might want to review some guidelines by the FTC in spotting the crooks.

It is becoming more common now with Garcinia, so beware, and read some of our reviews of brands like Ultra, Extreme, Purely Inspired, Miracle, Whole Body, Natural, and Pure Garcinia Cambogia.

Amazon is super convenient, and great at making sure you get what you order. But they don’t do anything to ensure the quality of a product.

Any brand that just popped up yesterday and will be gone tomorrow is NOT concerned with quality.

DR OZ WARNS ABOUT FAKE PRODUCTS

There are now dozens of new “Brands” of Garcinia Cambogia sold on Amazon that just make up a name and throw a label on some garbage product. And, they LIE about what is in the bottle!

The following quote is directly from the Dr Oz website where they warn about such deceptive marketing.

Screenshot 2016-04-02 04.52.52

This doesn’t mean all products sold on Amazon are bad. It just warns that products sold ONLY on Amazon are a much higher risk for being very poor quality.

[box]
Conclusion: Beware any Brand or Product that is sold exclusively online and not in a brick in mortar store. Those that exist only on Amazon and do not even have a website of their own are very likely to sell a very poor quality product.
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WHAT WE RECOMMEND

[product_category category=”garcinia-cambogia-2″ columns=”3″ per_page=”6″ orderby=”menu_id” order=”desc”]

CONCLUSION

For Weight Loss, we are convinced that:

The Ketogenic Diet(47,48), preferably combined with Intermittent Fasting is the most effective way to lose weight.

High Intensity Interval Training (HIIT) can greatly increase your metabolism to make weight loss easier and faster.

As for Garcinia Cambogia, the evidence shows that:

  • Garcinia Cambogia is NOT A MAGIC PILL that will melt the fat off
  • Garcinia Cambogia CAN HELP you lose a few more pounds a month

Time Restricted Feeding: Your Solution to Longevity and Shredding Fat

Why do we eat the way we eat? For health? Marketing? Societal standards? Or just because that’s the way we have always done it? If your answer is the last one, please never use that as a reason ever again.

With breakfast, lunch, dinner and grazing for snacks throughout the day; we could be eating for a 16 hour window. Increasing research is showing that we should narrow that window and give our body a chance to reset and cleanse itself. Let’s introduce time restricted feeding.

What is Time Restricted Feeding?

Time restricted feeding is not a way of telling you WHAT to eat, but a system of telling yourself WHEN to eat. Some people have referred to this as intermittent fasting, but the researchers who coined TRF thought feedingwould seem more inviting than the scary fasting word.

The time constraints of Time Restricted Feeding vary anywhere from a 12 hour eating window, an 8 hour eating window, all the way to 4 hours and fasting for 24 hours. The window starts when you first ingest something that isn’t toothpaste and ends when you have your last bite or sip of beverage that isn’t water at the end of your day. We will touch on those basic time frames further down, but the minimum effective dose is usually between 12 and 10 hours of eating per day.

Matching this time with your circadian rhythm and internal clock also looks to be beneficial. Your eating clock starts the moment you ingest something that isn’t water. For most of us, that would be our first cup of coffee in the morning. Holding off on that first bite, or sip allows you to start your feeding segment a bit later in the day.

It is suggested to try your best to halt your eating window before 7pm, so that your body can properly digest your food before entering your sleeping and fasted state. In all reality, do we want to eat a huge meal and then lie down for 7–8 hours? How silly does that sound?

What Are the Benefits?

1. Easier Implementation

Once we get over the idea that we need to eat every three hours, adapting to this schedule of eating overshadows any other diet or routine. This is a behavior based adjustment, not a complete overhaul of your eating or physical activity habits. Just do what you normally do and shorten the window.

“Diets are easy in the contemplation, difficult in the execution. Intermittent fasting is just the opposite — it’s difficult in the contemplation but easy in the execution.

Most of us have contemplated going on a diet. When we find a diet that appeals to us, it seems as if it will be a breeze to do. But when we get into the nitty gritty of it, it becomes tough. For example, I stay on a low–carb diet almost all the time. But if I think about going on a low–fat diet, it looks easy. I think about bagels, whole wheat bread and jelly, mashed potatoes, corn, bananas by the dozen, etc. — all of which sound appealing. But were I to embark on such a low–fat diet I would soon tire of it and wish I could have meat and eggs. So a diet is easy in contemplation, but not so easy in the long–term execution.

Intermittent fasting is hard in the contemplation, of that there is no doubt. “You go without food for 24 hours?” people would ask, incredulously when we explained what we were doing. “I could never do that.” But once started, it’s a snap. No worries about what and where to eat for one or two out of the three meals per day. It’s a great liberation. Your food expenditures plummet. And you’re not particularly hungry. … Although it’s tough to overcome the idea of going without food, once you begin the regimen, nothing could be easier.”

— Dr. Michael Eades

2. Decrease Body Fat

In it’s simplest description, TRF keeps the bad weight off and keeps the good weight on. While using an eating schedule, it is much easier to decrease body fat and maintain or increase lean muscle mass.

This all plays on our insulin levels. After you eat something, your insulin levels rise. Insulin is a hormone that’s made by the pancreas, which is used to regulate your blood sugar. It’s job is to take up the glucose that comes from sugar or carbs and either use it for energy or store it for later use. When you don’t eat for an extended period of time, say 8 to 12 hours or so, you enter a fasted state, your insulin levels are low, and your body starts to use fat as it’s source of energy.

Most people who only implement this schedule, with no other change to diet or exercise, tend to lose body fat because of this timing.

3. Reduces Chance of Cancer and Metabolic Disease

Occasional caloric restriction and fasting have been key weapons in the fight against cancer and metabolic disease. There hasn’t been tons of research on these issues, but the future looks bright.

One study fed rats a high fat diet, put them on a time restricted feeding program, and didn’t reduce calories. This protocol helped to prevent metabolic disease in this group versus the control group.

Dr. Dom D’Agostino, a researcher and professor at USF, focuses on the ketogenic diet and metabolic therapies. One of his suggestions for those heading to chemotherapy is to implement a fast beforehand to increase the benefits and help ward off the crappy after-effects.

4. Increases Lifespan

We can mention again, caloric restriction has been shown to increase the years of your life. When you are in a fasted state, your body looks for ways to keep you alive.

I don’t think many of us want to go on week long fasts to live a couple years longer. Let’s enjoy the years we have on this earth while lengthening when we can.

Good news for us is that time restricted feeding activates many of the same mechanisms that caloric restriction activates. We can have our cake and eat it too, within proper time frames…

5. Increases money in your wallet and time in your day

When I first implemented TRF into my lifestyle, I found so much more time and dollars lying around. You are essentially wiping out one meal from your old schedule. Gone were the Cheerios in the morning or the late night pizza. Want to be creative? Need more hours? Implement a time restricted feeding schedule and watch yourself come alive.

Popular Eating Schedules

16:8 This is quite possibly the most popular eating schedule in the intermittent fasting world. It allows for an 8 hour eating window usually starting with a late lunch and dinner. Skipping breakfast is easier for most because lunch and dinners seem to be the most social times for meeting up and eating together.

14:10 This is the window prescribed by Dr. Rhonda Patrick and the one she utilizes on most days. It’s essentially the largest feeding window you can get away with to realize the benefits. It accounts for 10 hours of eating and 14 hours of fasting. She wakes up and starts her window while ending with an early dinner or late lunch.

18:6 Want to one up the 16:8 community, here you go.

20:4 Some folks go for one BIG meal, usually dinner, and opt for FEASTING during this time.

24:0 or 24 Hour Fast You can implement a 24 hour fast once or twice a week to see benefits of decreasing your insulin levels for extended time. This usually can be done by eating dinner, then fasting until dinner the next day. Just make sure your time is used up and you’re not sitting around all day thinking about eating…

You Are an Experiment of 1, See What Works for You

The biggest takeaway anyone can glean from this post, I hope, is that you are your own experiment. Don’t let society, your family, or anyone else tell you what is right FOR YOU. Time Restricted Feeding has more and more research showing the positive effects, but it might not be right for you. Maybe you think you can get into 14:10 or 16:8 eating windows, GREAT! Maybe you want to try a 24 hour fast, that’s awesome. Lean into the edges of your comfort zone and see what happens. Many people are reaping the benefits of TRF, and you could be the next.

Why fasting matters: IGF-1 and inflammation

A very interesting and well designed intermittent fasting (IF) study published last year (hereafter denoted as “this study”) has been widely discussed because of its results on body composition. However, the data in this study shows a lot more if you are interested in health and longevity.

There is some debate in the calorie restriction (CR) community about the effects of IF in humans (as rodent data is mostly supportive of an independent effect). Overall, and currently, there are some major points that are thought responsible for the beneficial effects of CR, besides energy restriction per se. One of the most important ones is protein intake. There was a shift in the average thinking on dietary protein for some long-term CRONers over the years as to what the optimal intake of dietary protein is.

This is based mainly on the effect of protein (specially from animal origin) on IGF-1 levels, as high IGF-1 levels have been associated with increased risk of cancer. This was particularly troubling considering that protein intake directly regulates IGF-1 levels: in long term CRONers, a reduction of protein intake was necessary to lower serum IGF-1 levels.

This means that, in contrast to rodents, energy restriction was not sufficient to lower IGF-1. Further evidence of the effects of dietary protein come from studies done on Drosophila, which show that protein (but not energy) restriction was critical for the beneficial effects on longevity. Similar findings in rodents have also been published. I think there are some caveats and nuances to take into account, but that is a topic for another day.

So, in humans, long term CR appears to show most of the health benefits observed in other species, with the exception of lower IGF-1 levels. Thus, the current trend is to restrict protein intake to up to 0.8g/kg of body weight.

To quote Fontana et al., 2008 (my emphasis):

(…) our findings demonstrate that, unlike in rodents, long-term severe CR does not reduce total and free IGF-1 levels in healthy humans if protein intake is high. In addition, our data suggest that chronic protein intake is more powerful than calorie intake in modulating circulating IGF-1 concentration in humans. (…) these findings underscore the importance of dietary macronutrient intake in regulating metabolic events, and suggest that reduced protein intake may become an important component of anti-aging and anticancer dietary interventions, due to the importance of IGF-1 in the biology of aging (…) and in the pathogenesis of many human tumors.

Moro et al. studied the effects of an IF 16/8 schedule (16h fast, 8h eating window) or 3-meals-per-day (control) in resistance-trained subjects for 8 weeks. Although the IF group lost body fat and gained fat-free mass, the most interesting bit is in the blood markers measured. I will focus mainly on IGF-1, but it is worth mentioning that overall, markers improved dramatically in the IF group.

As the IF group consumed 1.93g of protein per kg of body weight and total calories were not restricted (they were around maintenance with approximately 14.97 kcal/lb of body weight and were not statistically different than in the 3-meals-per-day group), one can assume that the changes in several parameters are the result of the restriction of calories to a shorter window of time during the day. In other words, the design of this study helps us dissociate the effects of CR and protein intake from that of fasting or time-restricted feeding.

What happened with IGF-1 levels? They went down significantly, despite consuming a high protein and a normocaloric diet. In the IF group, IGF-1 levels (ng/mL) fell from 216.94 ± 49.55 to 188.90 ± 31.48, while in the control group (shown as “No IF” below) it didn’t change much (from 215.59 ± 56.25 to 218.41 ± 42,24). Just restricting calories to an 8 hour window reduced serum IGF-1 levels by 13% in 8 weeks despite consuming maintenance calories and high protein.

IGF-1 levels pre and post intervention in the 16/8 group (IF) and normal 3-meal per day pattern (No IF).

If we consider the proposed cancer risk that carries consuming a high protein diet (which in itself is controversial but not far-fetched in certain contexts), IF seems to promote “healthier” IGF-1 levels than spreading calories throughout the day.

We can also compare the effect of IF + resistance exercise + high protein/normocaloric diet (IF+EX) to the effect of CR without IF* on IGF-1 levels. After 8 weeks of IF + EX, IGF-1 levels were around 188.90 ng/mL, while after 6 years of CR, levels are around 194 ng/mL. I would argue that the difference is neither significant nor meaningful. But it shows that in humans, IF might be a more viable way of reducing high serum IGF-1 levels than CR (without protein restriction).

IGF-1 levels have also been shown to be responsive to a low calorie, low protein fasting-mimicking diet (FMD). The last study showed a 13% reduction after 3 months (or 3 cycles of 5 days of FMD), whereas a previous pilot studyshowed a reduction of 15%. Overall, reduction either by a 5-day per month FMD or by a 16/8 IF-high protein protocol seem to be comparable. Whether a larger fasting window (or a shorter eating window) promotes additional reductions is unknown. Probably combining IF + CR is synergistic.

An important point to mention is that its not a matter of “how low” you can go: low and high IGF-1 levels are both detrimental. One should look for the optimal serum level. Unfortunately, there is no consensus and the “optimal” level is unknown. Sufficient to say that IGF-1 levels per se are meaningless if not coupled to optimization of other markers (ie. insulin), but that is beyond the scope of this post.

Finally, concerns about lower serum IGF-1 levels being detrimental for muscle mass gains are based on a misunderstanding of physiology (which goes in line with the “more is better” mentality of some). Serum IGF-1 levels are not correlated with skeletal muscle hypertrophy (see also here), which is also exemplified in the study discussed here (no difference in muscle mass gains between groups despite lower serum IGF-1 levels).

This is because of differential expression and protein content/signaling in muscle vs liver (the latter is reflected in serum). Simply put: what matters for muscle hypertrophy is the IGF-1 available in muscle (not correlated to serum IGF-1), which is mostly produced locally and acting in an autocrine/paracrine manner.

*It is not stated whether CRONers in the Fontana, et al. study also fasted regularly, but based on most plans I’ve seen (and guides by the CR Society), food is spread during the day, in contrast to what happens in mice undergoing CR.


Inflammation

Initially I was going to make a different post about it, but it made sense to just add it to this one. Besides significant reductions in glucose and insulin levels, all markers of inflammation (IL-6, IL-1b, TNF-a, leptin) went down and adiponectin (anti-inflammatory) went up. You can see the values compared to the 3-meals-per-day group below:

Levels before the intervention are shown as black bars, while post-intervention, in white bars.

As these are markers associated with inflammation but also adiposity, can’t these results be explained by the loss of bodyfat in the IF group?

Unfortunately there is not much information on adipocytokines in lean populations in the absence of weight loss. But we can compare the magnitude of change with respect to body fat loss in obese subjects after a weight loss diet. In obese women, 3 weeks of a very-low calorie diet which reduced bodyfat by 3 kg, decreased IL-6 and leptin but no change was seen for TNF-a (and there are mixed results on the effect of weight loss on the latter). A reduction of TNF-a has been seen in obese subjects with a calorie restricted diet (-500 kcal), sibutramine and exercise. Achieving 10% of weight loss through an aggressive weight loss program (500–1000 kcal of restriction) in obese women decreased IL-6 by 27%, compared to around 19% observed for IF subjects. Overall, it looks like the reduction in inflammatory markers is not proportional to the amount of body fat lost (1.6 kg) in this study. This suggests a different effect of IF per se.

As before, the most relevant comparison could be to long-term CRONers. Adiponectin levels in people practicing sever CR for approximately 7 years have been shown to be around 15.7 ug/mL, compared to 13.9 ug/mL seen after 8 weeks of IF. In comparison, long-term endurance runners had lower levels (11.1 ug/mL) which is more or less the values observed for the No IF group in this study (10.9 ug/mL) (which can also serve as a resistance-trained control group, as they were experienced lifters). Importantly, these levels are comparable to those of matched sedentary controls consuming a typical Western diet (WD) (9.5 ug/mL). This suggests that fasting and CR are better for increasing serum adiponectin levels than exercise (endurance or resistance), being CR the most efficient. The lack of effect of exercise on adiponectin levels has been shown before. There is also some evidence that moderate weight loss does not result in higher adiponectin levels in obese subjects (see also here).

On the other hand, we can also compare the effect of IF or CR on IL-6 levels: CRONers showed significantly lower levels of serum IL-6 (0.73 ng/L) compared to IF subjects in this study (1.08 ng/L). Endurance runners also showed lower IL-6 levels (0.71 ng/L) than IF subjects. Disturbingly, those sedentary on a WD had almost the same levels (1.21 ng/L) as resistance-trained subjects in this study (1.33 and 1.24 ng/L before the intervention).

Chronic low-grade inflammation has been implicated in several diseases related to obesity and insulin resistance, in which adipocytokines play a major role. As described here, levels of these pro-inflammatory cytokines are related to cardiovascular disease:

Interleukin‐6 (IL‐6), interleukin 1b (IL‐1b) and tumour necrosis factor α (TNFα) are the principal pro‐atherogenic cytokines,1 which are also produced in tissues other than the vascular wall and immune system, such as adipose tissue, myocardium, intestine, etc.1 They upregulate the expression of adhesion molecules on vascular endothelium, depress nitric oxide synthesis and promote the subendothelial migration of leucocytes. Further to their local regulatory role at a vascular level, these cytokines induce the liver‐derived synthesis of acute phase proteins, such as fibrinogen, plasminogen, C‐reactive protein (CRP) and serum amyloid α (SAA), which amplify inflammatory and pro‐coagulant responses.

The importance of the molecules described above can be further seen in this review. Some extracts below (my emphasis):

Adiponectin

Adiponectin has also been reported to have antiatherogenic effects (Funahashi et al. 1999, Ouchi et al. 1999). In addition, adiponectin exhibits cardioprotective activity in ischemic heart disease through AMPK and cyclooxygenase 2 pathways (Shibata et al. 2005). (…) Adiponectin also has anti-inflammatory effects that contribute to its protective role against metabolic stress in obesity. Adiponectin suppresses TNFα production in obese mice (Xu et al. 2003a), and adiponectin-deficient mice have high levels of TNFα in adipose tissue (Maeda et al. 2002). Low levels of plasma adiponectin are associated with C-reactive protein in humans (Ouchi et al. 2003). Adiponectin enhances the clearance of apoptotic cells by facilitating their opsonization and uptake by macrophages (Takemura et al. 2007). Some of the anti-atherogenic effects of adiponectin are also mediated by its role in the suppression of inflammatory responses. Adiponectin inhibits nuclear factor-κB (NFκB) activity and its downstream adhesion molecules leading to reduced monocyte adhesion to endothelial cells (Ouchi et al. 1999, Okamoto et al. 2002). In addition, adiponectin confers vascular-protective activities by suppressing the apoptosis of endothelial cell (Kobayashi et al. 2004).

Leptin

Leptin is structurally similar to Class I helical cytokines and shares the same JAK–STAT pathway downstream of its receptor. Leptin expression can be induced by endotoxin or cytokine TNFα (Grunfeld et al. 1996). Conversely, leptin increases thymic secretion of acute-phase reactants and TNFα and promotes T helper 1 cell differentiation (La Cava & Matarese 2004). Leptin acts on T cell, macrophages, and other immune cells to stimulate the production of a wide spectrum of cytokines (La Cava & Matarese 2004). In light of the role of several cytokines in enhancing energy expenditure and suppressing food intake (Ye & Keller 2010), this proinflammatory action of leptin might contribute to its overall effects in body weight regulation.

TNF-a

TNFα was the first cytokine identified in the adipose tissue of obese mice, marking the start of the metabolic inflammation concept (Hotamisligil et al. 1993). The direct involvement of TNFα in obesity-induced insulin resistance was confirmed by observations that TNFα treatment interferes with insulin signaling and blocks insulin actions (Hotamisligil et al. 1994). Mice lacking the functions of TNFα or its receptors are protected from obesity-induced insulin resistance and hyperglycemia (Uysal et al. 1997, 1998). It was initially thought that adipose-derived TNFα was produced mainly by adipocytes, but the parallel trend of macrophage infiltration and TNFα expression in adipose tissue of obese mice suggests that a significant portion of the adipose TNFα pool might be derived from macrophages and other immune cells. Interesting, FFA strongly stimulates TNFα production in macrophages (Nguyen et al. 2005) and in turn, TNFα stimulates lipolysis to increase fatty acid release from adipocytes (Wang et al. 2008). This FFA-cytokine cycle suggests that metabolic inflammation, once started, can use this self-perpetuating mechanism to further its inhibitory effects on insulin signaling and energy metabolism. In addition, TNFα directly stimulates hepatic lipogenesis in vivo (Feingold & Grunfeld 1987), and adipose-derived TNFα is also a major mechanistic link between obesity and cancer (Park et al. 2010).

IL-6

IL6 is one of the major pro-inflammatory cytokines whose expression level increases in the adipose tissue of obese mice and patients, but its role in glucose metabolism has not been fully resolved. (…) There are several potential explanations for the seemingly contradictory data regarding IL6 in insulin action and glucose metabolism. Effects of acute vs chronic treatments need to be differentiated and dose and site of action of IL6 need to be carefully considered. In addition, IL6 produced by different organs might also contribute to its complex effects on metabolic regulation.

From an in-depth review of IL-6 and metabolic inflammation, please read here. Although its not clear if IL-6 has a direct causative effect (it can have pro and anti-inflammatory effects), it has been associated with the T2DM, CVD and inflammation:

Low-grade chronic inflammation in obesity, reflected by a two- to threefold increase in the systemic level of cytokines including IL-6, appears to precede and is a risk factor of the subsequent development of insulin resistance and T2DM (Spranger et al., 2003; Wang et al., 2013; Lowe et al., 2014). (…) IL-6 has been identified as an independent predictor of T2DM and associated cardiovascular events (Spranger et al., 2003; Lowe et al., 2014). Adipocytes and macrophages residing in adipose tissue are the major sources for the elevated plasma IL-6 concentration up to 2–3 pg·mL−1 in patients with obesity and T2DM (Pradhan et al., 2001; Spranger et al., 2003). Nevertheless, the existing evidence is not enough to establish a causal association between IL-6 levels and the progression to metabolic and cardiovascular disorders. Due to its pleiotropic actions in various tissues and organs, the exact role of IL-6 in the pathogenesis of diabetes must be examined carefully in a cell- and tissue-specific manner, but allowing for the possibility of crosstalk between affected tissues and organs.


Overall, it seems that restricting calories daily to a short window of time might be metabolically beneficial in the absence of significant calorie or protein restriction. In combination with a diet with adequate protein and resistance exercise, it seems to promote favorable changes in body composition and improve metabolic markers related to inflammation. The combination of IF and CR might be synergistic, while the effects of longer daily fasting periods with a shorter eating window is unknown.

Let’s see at the body composition data from the study.

  • The IF group lost 0.9 kg in 8 weeks. This represents 1% of body weight. They lost 15% of body fat mass.
  • In kcal/lb (a rough measure of energy intake level), at the end of the study, the IF group was consuming around 14.97 kcal/lb, while the control group was consuming 15.47 kcal/lb. Generally, a good estimate for maintenance calories is between 14–16 kcal/lb.
  • In the IF group, subjects went from consuming 2826 to 2735 kcal/day. In the control group, it went from 3007 to 2910 kcal/day. There was no significant difference between calorie intake between groups. But for the sake of the argument, lets say that they were in calorie deficit. Energy restriction was thus 3% from baseline in both groups. This level of restriction is well within errors in estimation and in all practical purposes, not considered as “energy restriction”. However, if we assume that it indeed is considered an energy restricted diet, then no one can argue that the deficit was small and almost non-significant. This also agrees with the small amount of weight loss, which is well within normal daily variation.
  • Protein intake was increased compared to baseline and not significantly different between groups (1.93 g/kg in the IF group vs. 1.89 g/kg in the control group).

Based on the above, one can rely on the lack of statistical significance in energy intake between groups and mean calorie intake per day to assume that both groups consumed the same number of calories, which were around maintenance. However, the calorie difference might be biologically significant as suggested by the greater loss of body fat in the IF group. Given that the focus of the criticism is in the latter, I will consider the IF group to be in a slight calorie deficit and show how it doesn’t change the main argument of the original post.

What we know about IGF-1, calorie restriction (CR) and weight/fat loss

As mentioned in the other post, it is well established than in humans, dietary protein intake is the main determinant of serum IGF-1 levels. So in theory, the higher the protein intake, the higher the IGF-1 levels. CR has a modest effect. On the other hand, CR, by definition, will result in weight loss, which could also modulate IGF-1. Thus, the significant reduction of IGF-1 in the IF group, if not because of the temporal restriction of food to a short window, could be due to:

a) Lower protein intake than the control group.

b) Lower caloric intake or greater CR than the control group.

b) Greater weight/fat loss than the control group.

Protein intake was not different between groups and was high, so if anything, it should have increased IGF-1 levels.

The CR level in both groups was 3%, so the level of restriction for both was the same (the absolute level of restriction was 91 kcal for the IF group and 97 kcal for the control group). The difference in basal energy intake between groups was due to different initial mean body weight, which was not statistically significant (83.9 kg in the IF group vs. 85.3 kg in the control group), but at the end of the study was 175 kcal. Again, the difference was not statistically significant, both diets were on maintenance levels and restricted from basal levels by the same amount. But for the sake of the argument, we will assume that this difference could account for the change in IGF-1.

The IF group lost significantly more body fat than the control group. Thus, it could also be that this loss of body fat explains the difference in IGF-1 between groups.

In summary and for further comparisons, the IF group was 3% CR, lost 1% of body weight and lost 15% of body fat mass in 8 weeks. The appropriate way to calculate the calorie deficit should be to subtract the intervention calories from basal calories (which is 91 kcal), but as people have focused on the 175 kcal difference with the control group, we will use this number as the calorie deficit (-175 kcal).

Because CR and weight loss are invariably linked, I will discuss them together.

I already mentioned that long-term (6 years) CRON results in a modest decrease in IGF-1, with average levels compared to what achieved in 8 weeks in the IF group. This population is the most relevant for discussion of independent effects of CR on metabolic markers as they are weight-stable (so no confounding due to weight loss).

There is also data from the CALERIE study, at 1 and 2 years. In this intervention, normal weight subjects were calorie restricted for 2 years to a goal of 20% CR. After 1 year, subjects achieved only 12% of CR (-279.5 kcal), reduced body weight by 10.7%, fat mass by 24%, improved insulin sensitivity and some inflammatory markers, but didn’t reduce IGF-1 significantly. The same results were seen after 2 years: body weight was reduced by 10.4%, fat mass by 22.5% with a similar CR level (-216.3 kcal), but IGF-1 levels were only reduced by 8.6%. Importantly, protein intake increased in this period to 1.28 g/kg.

I have put these differences in a table to make it easier to compare:

All changes are with respect to baseline values and just a rough difference between means.

Achieving 10% of weight loss, 22.5% of fat loss and 10% CR in 2 years didn’t produce the same reduction in IGF-1 as 8 weeks with IF with 3% CR, despite higher weight/fat loss and lower protein and calorie intake. Even if we consider that the calorie reduction was 175 kcal (which was not), it still falls short compared to that in Fontana et al., 2016 (175 kcal vs 216 kcal, or 6% CR vs 10% CR).

I believe the most adequate comparison is the one above, because it compares normal weight subjects. But there is also data from obese subjects undergoing weight loss.

In overweight women, 25% of energy restriction either continuously (CER, 1500 kcal daily) or intermittently (IER, 647 kcal for 2 days per week) resulted in similar body weight loss after 6 months. Neither of the interventions reduced significantly IGF-1. However, there is a clear trend in the IER group for reducing IGF-1 levels (baseline=201.3; 6 months=191.6 ng/mL) that was not seen in the CER (baseline=202.9; 6 months= 203.7 ng/mL) and didn’t appear to correlate with weight or fat loss.

But the IER protocol is more similar to the 5:2 diet than to a 16/8 IF protocol (and it involves less overall fasting period). Nevertheless, it shows that 6 months of 25% CR that produced significant changes in body weight and fat loss didn’t reduce IGF-1 levels. Similar results have been observed by the same authors: no change in IGF-1 with 25% daily or intermittent energy restriction despite significant weight/fat loss.

In other group of obese subjects, dietary restriction (1200 kcal/day) increased IGF-1 levels after 8 weeks but returned to baseline after 16 weeks, despite 5.8 and 8.1 kg of body weight lost (8 vs. 16 weeks, respectively). A similar increase in IGF-1 after weight loss has been observed in other study with obese women, as well as in an intervention with or without orlistat.

As described, there is no clear relationship between body weight/fat loss and degree of CR on serum IGF-1 levels in normal or obese subjects. Only after a long period of time (2 years) and constant, significant CR (10–12%) a small change in IGF-1 is observed. Thus, it is highly unlikely that the change seen in the IF group is due to either CR or weight/fat loss, specially with a high protein intake, almost no CR and short duration of the intervention (8 weeks).

Even if one assumes that the IF group was in significant calorie deficit, the degree of IGF-1 reduction in such a short time and with the amount of protein is remarkable. As mentioned in the other post, comparable reductions have only been observed after 3 cycles of a Fasting-Mimicking Diet(13%) or reducing protein from 1.67 g/kg to 0.95 g/kg for 3 weeks (22%), the latter being the most effective.

Finally, I want to mention something important that was not part of the original post as the study didn’t measure it: IGFBP (IGF-binding proteins). The activity of IGF-1 depends on its bioavailability, which in turn is determined by the ratio of IGF-1 to IGFBP (IGF-1:IGFBP ratio).

Simply put, the concentration of IGFBP determines the amount of free serum IGF-1, which in the end is the available hormone in circulation. 2 years of CRincreased IGFBP-1 (one isoform of IGFBP that is regulated by metabolic status) by 20–25%, which in turn reduced the IGF-1:IGFBP-1 ratio by 42%. So even though CR didn’t reduce IGF-1 significantly, it did reduce the amount of free IGF-1.

Why it makes sense

Quoting Fontana et al., 2016 (my emphasis):

In fact, serum concentration of IGFBP-1, unlike IGFBP-3 which binds 75–90% of circulating IGF-I, is heavily influenced by the metabolic (i.e., insulin resistance, and insulin and glucagon levels) and nutritional (fasting and refeeding) state of the individual. Excessive adiposity-induced insulin resistance and compensatory hyperinsulinemia have been shown to decrease hepatic synthesis of IGFBP-1, which translates into increased concentrations of bioavailable IGF-1, without modifications in serum total IGF-1 levels (Lukanova et al., 2001; Maddux et al., 2006).

Patients with type 1 diabetes have higher serum IGFBP-1 concentrations than normoglycemic controls (Suikkari et al., 1988), and acute steady state hyperinsulinemia lowers serum IGFBP-1 levels by 40–70% in normal individuals (Yeoh & Baxter, 1988; Snyder & Clemmons, 1990). Moreover, it has been shown that circulating levels of IGFBP-1 are acutely increased by 3–4 fold in response to overnight fasting and decline rapidly after a meal (Busby et al., 1988; Smith et al., 1995).

Indeed, IGFBP-1 has been proposed as a marker of hepatic insulin sensitivity. While IGF-1 levels are primarily determined by dietary protein intake, IGFBP-1 levels are regulated by insulin secretion. It appears that fasting decreases IGF-1 and increases IGFBP-1, effectively reducing IGF-1 bioavailability. In normal subjects after 36 hours of fasting, IGF-1 levels are reduced from 249.5 to 219.4 ng/mL (-12%) and IGFBP-1 levels are increased from 27.4 to 205.2 ng/mL (+649%).


A note on adipocytokines

In the previous post I presented evidence that the relationship between weight loss and levels of adipocytokines is equivocal. However, I found information on TNF-a in non-obese subjects. From the same CALERIE study, TNF-a was reduced by 22% after 2 years, compared to only 8% in the IF group, which is almost the same reduction observed for the CR subjects in CALERIE after 1 year (8.5%) with a higher CR level. Still, absolute values are significantly lower in long-term CRONers.

Steps to Lower your Blood Sugar levels and live longer

This article was written and published on GarmaOnHealth.com by Joe Garma, and has been reproduced here in its entirety.

There’s more than a 3-in-4 chance that your blood sugar is too high, and this can lead to a number of chronic health issues, even shorten your life. Learn how to measure and fix your blood sugar. The Apple Watch, FitBit Ionic and Epic Health lead the way.

fix your blood sugar

 

THERE’S A race to perfect technologies that can continuously monitor blood sugar levels without the need to prick your finger for a blood sample to be “read” by a glucose monitor. This is great news for health freaks, people with pre-diabetes or full blown diabetes my have to do up to 3,000 times a year.

Ouch!

You can imagine the flood of business that a company could attract if it could create a non-invasive, less bloody way of testing for blood sugar. Many are trying.

A few weeks ago, I wrote about Apple’s effort to make its Smart Watch seamless track blood sugar through an innovative sensor, and now I’m going to add Fitbit’s smartwatch and Epic Health’s phone app to the mix.

I don’t have to go too far out on a limb to suggest that monitoring your blood sugar is a very good idea simply because:

  1. It’s very likely that yours is too high; and
  2. High blood sugar is very unhealthy.

I can make the first assertion because, as you’ll soon see, studies show that more than three-quarters of us have blood sugar levels that are too high.

I can make the second assertion because medical science has proven that sustained high blood sugar levels is bad for metabolic health, brain health and a long, healthy lifespan.

So, let’s take a peek at the new Fitbit and Epic Health technologies, then get a sense of how you can assess if you have a blood sugar problem without any measuring device, and finally what you can do to fix your blood sugar; meaning, lower it to a healthy mark.

In this article, you’ll discover:

  • Two new blood sugar testing technologies;
  • The ideal fasting and post-meal blood sugar levels;
  • A subjective test to indicate that your blood sugar is too high; and
  • How to fix your blood sugar.

Let’s dive in…

Two New Blood Sugar Testing Technologies

As will see below, it’s not absolutely necessary to be able to measure in order to fix your blood sugar, assuming it’s too high, but it sure takes the guess work out of the equation.

Of the two new blood sugar testing technologies I want to tell you about, one’s a smart phone + app that may be available in months; the other is a smart watch available real soon (pre-orders solicited).

The Epic Health App

Epic Health blood monitoring app

A new app called Epic Health is well on the way to perfect a new way to control blood sugar without the need for painful monitoring via glucose monitors. The objective is to monitor glucose levels in healthy and type 2 diabetic patients is just as accurate as traditional, invasive methods that use the finger prick test to draw blood. It’s designed to make blood glucose monitoring less intrusive and more engaging, encouraging users to understand how certain foods affect their body.

The app, which works by the user place a fingertip over the camera lens of their smartphone, has held its first few weeks of pre-clinical trials in Hereford, England, which are being conducted to ensure that the app can accurately measure glucose when compared to methods when blood is drawn.

So far, testing results show that a mobile phone application can accurately estimate blood glucose levels of healthy, diagnosed and borderline type 2 users. The application has also proven that healthy subjects can use it to monitor their blood glucose variations after drinking, eating or even exercising, which will encourage keeping a healthy lifestyle.

Keep up with this technology and when it may become available here.

The Fitbit Ionic Smartwatch

 

Fitbit Ionic Smartwatch introduces a blood oxygen sensor

You probably have heard of Fitbit. As the BBC reports, until recently, Fitbit was ranked the world’s bestselling wearable tech brand, but nothing lasts forever — market research firm IDC reported in June that it had been overtaken by both Xiaomi and Apple in terms of shipments over the first three months of the year.

It could be, however, that Fitbit is going to regain its former glory with its new, Fitbit Ionic Smartwatch introduces a blood oxygen sensor that estimates the amount of oxygenated hemoglobin in blood.

Fitbit has started accepting pre-orders, it has said shipments will not start until late September.

 

The Blood Sugar Sweet Spot

Apple, FitBit and Epic Health, among others, are racing to perfect a non-invasive way to measure blood sugar simply because keeping your blood glucose levels as close to normal as possible can be a lifesaver. Tight control can prevent or slow the progress of many complications of diabetes, giving you extra years of healthy, active life, says Diabetes.org.

The question is what is “normal”?

The following two graphs tell me what I want my normal to be, and that’s less than 85 mg/dL for fasting blood sugar.

The graphs indicate how blood sugar rises with age and how lifespan is related to blood sugar levels. Notice how the groups that live longer have lower blood sugar at the same age than their shorter-lived peers. Even more interestingly, notice how in males that live at least 70 years, you can predict death more reliably by blood sugar level than you can by age.

 

 Lifespan (LS) Predicted By Blood Sugar, MalesLongevity Predicted By Blood Sugar, Males
Lifespan (LS) Predicted By Blood Sugar, Females

Longevity Predicted By Blood Sugar, Females

Not only can maintaining low blood sugar increase lifespan, but can help ensure your brain keeps pace.

New research has found blood glucose levels even at the normal range can have a significant impact on brain atrophy in aging.

As reported in Neuro Science News, the impacts of blood glucose on the brain is not limited to people with type 2 diabetes. Dr. Erin Walsh from the Centre for Research on Ageing, Health and Wellbeing at Australia International University, said:

People without diabetes can still have high enough blood glucose levels to have a negative health impact, [and those] with diabetes can have lower blood glucose levels than you might expect due to successful glycaemic [sic] management with medication, diet and exercise…

It helps to keep unhealthy highly processed and sugary foods to a minimum. Also, regular physical activity every day can help, even if it is just a going for walk.

My question for Dr. Walsh is what fasting and post-meal (“postprandial”) blood glucose number should we aim at maintaining?

Since the answer to that question wasn’t in Neuro Science article, let’s turn to the Life Extension Foundation for the answer. In Are We All Pre-diabetic, health journalist Kirk Stokel writes that people living in industrialized nations are experiencing an “epidemic of elevated blood sugar”:

The percentage of adults who suffer chronic high blood sugar is staggering! One report evaluated 46,000 middle-age individuals and found more than 80% had fasting blood sugar of 85 mg/dL or greater.

Another study involving 11,000 middle-age and older individuals showed more than 85% had fasting blood sugar of 85 mg/dL or greater.

Since incidence of disease starts to increase when fasting blood sugar rises above these levels, this means the vast majority of aging humans today endure chronic cellular damage associated with elevated blood sugar.

This epidemic of elevated blood sugar will accelerate age-related disease until the medical profession realizes that their test values for defining “normal” blood sugar are horrifically defective.

Notice that 85 mg/dL fasting blood sugar mark mentioned above? This is the mark that the Life Extension Foundation believes should be your maximum fasting blood sugar. If you want to fix your blood sugar, get it down to 85 or even a bit lower.

Scroll back up and look at the two blood sugar age charts again and notice that 85 mg/dL is pretty much as high as you want to be at age 50, and yet more than 80 to 85% of us have fasting blood sugar higher than that.

Nonetheless, mainstream medicine continues to accept as “normal” fasting blood sugar that’s well above optimum, which is between 70 and 85 mg/dL, says Kirk Stokel. Instead, your doctor is likely to believe that you are not “diabetic” unless fasting blood glucose exceeds 125 mg/dL, and that the range between 100 and 125 mg/dL is considered “pre-diabetic.” Having a blood sugar reading of 99 mg/dL, therefore, is likely to be acceptable by your doctor despite the potential dangers lurking within your body.

Not only does conventional medical wisdom get it wrong regarding ideal fasting blood sugar, doctors typically do not convey to their patients the risks of after-meal (postprandial) blood sugar spikes. If sufficiently high or sustained, these sudden surges in blood sugar that can occur after meals (particularly high carb meals) can damage delicate blood vessels in your brain, heart, kidneys, and eyes, as well as accelerate the aging of cells and tissues throughout your body.

Utilizing only fasting blood glucose readings does not detect perilous after-meal glucose spikes that present an increased risk of death. This is important to know, given that scientific research shows that after-meal spikes in blood sugar are potentially more damaging than elevations of fasting blood sugar.

In his article, Kirk Stokel annotates the research that indicates:

  • For people with “normal” blood sugars and “normal” glucose tolerance tests, the risk of a heart attack increases by 58% for each 21 mg/dL increase in after-mealblood sugar.
  • “Normal” after-meal glucose elevation can increase the risk of dying from cardiovascular disease by 26%, which underscores the need for control of after-meal glucose spikes, particularly as it relates to cardiovascular complications.
  • An isolated fasting glucose reading fails to provide information on glucose control throughout the day; therefore, a fasting glucose reading of, say, 95 mg/dL, this may be an artificially low number that does not reflect real world, all-day glucose status that may be considerably higher.

The bottom line is:

Without controlling fasting and postprandial sugar spikes, the stage is set for accelerated aging and a series of degenerative diseases.

OK, so now we know that sustained, high blood sugar is antithetical to good health and a long, robust healthspan, how can you tell if your blood sugar is too high, assuming you don’t have a FitBit Ionic Smartwatch, nor are pricking yourself throughout the day for drops of blood to be assessed by a glucose monitor?

Dr. William Cole has a few suggestions.

 

You Can Tell If Your Blood Sugar’s Too High

Before you can fix your blood sugar, it’s helpful to know it your fasting or blood sugar, fasting or postprandial is too high (or too low for that matter). To do that reliably, you need a way to measure it, which requires a glucose monitor or some other device, such as the forthcoming blood sugar monitoring Apple Watch or one of the two new technologies I address below.

But if your diet is dominated by one particular macronutrient, you may already have a sense if your blood sugar is too high, which brings us to Dr. William Cole’s article about “how to know if your blood sugar is out of whack”.

As a functional medicine expert, Dr. Cole’s focus is to discover the root cause(s) of health issues. If you crave and/or eat a lot of sugary food (think carbs) on a daily basis, it’s a pretty good indication that your blood sugar is too high. (Note that this isn’t true for everyone, as this Weizmann Institute study showed.)

What follow is Dr. Cole’s answers to four questions put to him about sugar consumption and blood sugar. My intention is for you to pick up on some tips to determine if your blood sugar levels may be too high simply by carefully considering how much sugary foods you regularly consume.

1. How many daily grams of sugar per day are healthy to consume? (Including naturally occurring fruit sugars & milk sugars)?

The answer basically depends on the sugar source and your individual tolerance to sugar.

Advice that is useful to most people includes:

  • Dramatically reduce or eliminate sugar from candy, pasta, white bread, and ice cream. Natural sugars in foods like sweet potato, berries or whole-milk yogurt are better tolerated because these foods contain other nutrients to balance out the glucose-spiking affect of sugar.
  • Try to eat carbohydrate foods that contain insoluble fiber, as it can’t be absorbed by the body and thus has minimal effect on blood sugar, perhaps even lowering it.
  • Be mindful of how your body reacts to carbs and note if you feel sluggish or sleepy after eating a carb-rich meal or snack
  • Stay below 50 grams per day of net carbs (total carbs minus insoluble fiber) of both added and naturally occurring sugars.

2. How does sugar affect hormonal balance?

When you eat sugar (and remember this includes all simple, non-fibrous carbs), your pancreas makes a hormone called insulin that is needed to regulate blood sugar and bring the post-food spike down back to normal after ingesting any type of sugar, whether it’s added or naturally occurring.

In its normal-functioning state, the release of insulin is a healthy, necessary response—it’s when you eat too much sugar and flood your body with insulin that things get out of whack and your blood sugar begins to have trouble regulating itself.

If you have normal, healthy insulin function, all is well; however, if your blood sugar is chronically unbalanced, it can directly affect the HPA (hypothalamic-pituitary-adrenal) axis, which controls your body’s release of cortisol and leads to adrenal fatigue.

Cortisol and blood sugar are positively correlated; meaning, when your blood sugar is high, cortisol is also high and vice versa. This is one of the top contributors to adrenal fatigue. Excess sugar is also inflammatory, which further feeds hormonal imbalance.

3. There is a lot of controversy about “natural” sweeteners such as honey, maple syrup, molasses, agave, and stevia. Are these sweeteners safe?

Dr. Cole says that honey, maple syrup, molasses, dates, and fresh fruit juice are among the best sweeteners you can use in limited amounts, and that stevia, xylitol, and monk fruit are also fine low-carb options, but can cause some digestive symptoms like bloating if eaten in excess. The key with all sweeteners, he says, is moderation!

It’s hard to argue with moderation, but my advice is to gradually wean yourself from added sweeteners. Our taste buds are malleable and trainable, and you can sensitize them to sweetness. Simply reduce the amount of sweeteners you take, say by 25% per week and in one month you’ll no longer miss the stuff.

4. How do you know if your blood sugar levels are out of whack? What impact does sugar consumption have on this, and how can you fix it?

There are quite a few symptoms that can point to a blood sugar imbalance such as:

  • Insatiable sugar cravings that just don’t go away even after consuming sweets
  • Missing a meal makes you hungry, lightheaded, and jittery
  • Trouble losing weight
  • Often thirsty
  • Urinate a lot
  • Blurry vision
  • Brain fog is experienced on a regular basis

Excess sugar consumption can amp up any of the above mentioned symptoms because of it can lead to insulin resistance and the inability for your body to use insulin properly to regulate blood sugar.

If you do have unbalanced blood sugar, you can do a number of things to fix it, from supplementing with magnesium, vitamin D, and chromium to increasing your probiotic intake to reducing your stress levels. And this is the topic of the next section

 

How To Fix Your Blood Sugar

At this point you know that their are some novel technologies underway that eventually will come to market and allow us to seamlessly and continuously monitor our blood sugar so we’ll be able to tell which foods have a modest affect on it, and which spike our blood sugar to unhealthy levels.

You’ve also been provided some tips to get a pretty good idea if your food choices are likely to amp up your blood sugar.

Now, let’s get into how to balance our blood sugar, again, courtesy of Dr. Cole who suggests the following natural ways to fix your blood glucose.

Get a lab test to find your baseline

These are the results Dr. Cole would like to see:

  • Serum insulin: Optimal Range: < 3 ulU/mL
  • C-peptide: Optimal Range: 0.8 to 3.1 ng/mL
  • Fasting blood sugar: Optimal Range: 75 to 90 mg/dL
  • Hgb A1C: Optimal Range: < 5.3 percent
  • Triglycerides: Optimal Range: <100 mg/dL
  • HDL: Optimal Range: 59 to 100 mg/dL
Drink Macha tea

The EGCG compound in green tea has demonstrated a stabilizing effect on blood sugar levels. Drinking the whole green tea leaf in the form of matcha powder will provide plenty of ECGC in your diet.

Take alpha-lipoid acid

In several studies, alpha-lipoic acid was helpful in balancing out blood sugar levels and improving insulin resistance. This antioxidant also strengthens immunity, improves energy in cells, protects brain cells against excitotoxicity, and removes excess toxic metals. Suggested dose for blood sugar control is 200 milligrams three times a day

Bump up magnesium

Research published in the medical journal Circulation followed nearly 5,000 people for 15 years, and found that people who took higher levels of magnesium had a decreased risk of metabolic syndrome. Another similar study, published in the American Journal of Epidemiology, followed more than 1,000 healthy adults for five years and saw that greater magnesium intake improved insulin sensitivity. Other studies have shown that magnesium improved triglycerides and high blood pressure—two other hallmarks of metabolic syndrome and diabetes.

Boost chromium

When chromium levels are low, HDL (the “good” cholesterol) levels fall, insulin resistance develops and triglycerides rise. Chromium supplementation has been shown to improve receptor function. The best food sources of chromium include onions, tomatoes, potatoes, and sea vegetables.

Increase Nrf-2

The protein Nrf-2 plays a role in regulating antioxidant gene induction. Nrf-2 actually turns on genes that are responsible for antioxidant and detox pathways. Inflammation is calmed when Nrf-2 is activated and tends to get worse when there are low levels of Nrf-2. Many dietary antioxidants have been found to activate Nrf-2, including:

  • EGCG from green tea
  • Quercetin from apples
  • Curcumin from turmeric
  • Resveratrol from grapes
  • Rosmarinic acid from rosemary
  • L-sulforaphane from broccoli
  • Thiosulfonateallicin from garlic
Add tocopherols

Fat-soluble tocopherol (also known as vitamin E) has been shown to support insulin sensitivity. Standard doses range between 600 and 900 milligrams.

Spice up

A bioflavonoid found in cinnamon called proanthocyanidin may alter the insulin-signaling activity in fat cells and help with diabetes. The spice has also been shown to significantly reduce blood sugar levels and triglycerides in people with type 2 diabetes.

Heal your gut

You gut health and blood sugar balance are connected. Metabolic disease can negatively affect your gastrointestinal system, and poor gut health can mess up your blood sugar. One study found that transplanting the microbiome of diabetic mice into healthy mice made them diabetic as well. Be aware that advanced glycation end products (AGE) are harmful compounds that have the potential to cause leaky gut, and read up on candida overgrowth, which is also linked to blood sugar problems.

Absorb the sunshine vitamin

In one study, supplementing with vitamin D for 12 weeks decreased body fat by 7%. Low levels are also linked to metabolic syndrome. The optimal range to aim for is 60 to 80 ng/mL.

Increase healthy fats

One study found that higher blood sugar in non-diabetics decreased function in areas of the brain affected by Alzheimer’s disease. This is one reason why Alzheimer’s is often referred to in the medical literature as “type 3 diabetes.” On the other hand, a ketogenic diet—where fat, not sugar, is your primary source of energy—has been shown to do some remarkable things for your brain health.

Healthy fats provide a slow, sustainable form of energy. For our brain to work properly, it requires lots of energy. And from a biological and evolutionary perspective, the most sustainable form of energy for optimal brain health is good, healthy fats.

Support methylation

Methylation is needed for healthy blood sugar balance. Activated B vitamins—like B9 L-Methylfolate (L-5-MTHF) and B6 Pyridoxyl-5-Phosphate (P5P)—are a great way to support methylation pathways. Food that supports methylation include spinach, okra, and turnip greens, and meats like chicken liver or grass-fed beef liver, which have the highest levels of bioavailable B vitamins.

Activate PPARs

PPARs are “peroxisome proliferator-activated receptors” and studies suggest they may help improve inflammatory conditions such as atherosclerosis, asthma, colitis, MS, and other autoimmune conditions. Some PPAR activators for you to bring into your life: wild-caught fish, green tea, astragalus, ginger, and sea buckthorn.

More omega

The ability of omega-3 fatty acids to lower the risk of stroke and heart attacks is well-known. Less known is that omega-3 fats in the form of fish oil convert the potentially harmful very low-density lipoproteins (VLDL), which are linked to diabetes, into less dangerous low-density lipoproteins (LDL). For more on this, Why Your LDL Cholesterol Particle Size Determines Your Heart Disease Risk and What To Do About It.

Give yourself some adaptogenic love

Adaptogens are adept at balancing hormones and inflammation. A study found the adaptogen American ginseng berry juice could significantly improve glucose tolerance and normal blood sugar levels after just 10 days!

That said, my research on the matter compels me to tell you about two other adaptogens that are potent blood sugar moderators, Berberine and Amla.  You can get the deep dive on these and more in my article, You Absolutely Need To Lower Your Blood Sugar, but suffice to say:

 

Your Takeaway

Remember these four points:

  1. Although your doctor might be satisfied if you’re fasting blood sugar is 100 ng/dL, medical experts who wade deep into the data say that it needs to be much lower if you’re to enjoy a long and strong life. Go for 85 ng/dL or lower.
  2. There will soon be various devices that will be able to continuously monitor your blood sugar without needing your blood. Right now Fitbit Iconic Smartwatch may fit the bill.  I suggest that before you buy it, do some research into third-party analysis of its effectiveness.
  3. Even without some objective device to track your blood sugar, you can get a pretty good idea of how well you fare by taking an inventory of the amount of sugary foods regularly consumed, and how you feel after eating them.
  4. Finally, there’s much you can do to fix your blood sugar, both fasting and post-meal levels. Scroll back up and choose a few foods and supplements that you’d be willing to try and then include them one by one into your diet.

If you know anyone that eats too much sugary foods — and you just flashed on two people — do them a favor and share this article with them.

 

This article was written and published on GarmaOnHealth.com by Joe Garma, and has been reproduced here in its entirety.

Starvation Mode: When You Eat Less, Your Body Burns Less

Besides storing fat, the body has several methods to survive periods of food shortage and starvation.

One of them is called adaptive thermogenesis, sometimes referred to as “starvation mode”.

It involves a reduction in the amount of calories your body burns, resulting in slower weight loss and faster weight regain.

It is defined as a decrease in resting energy expenditure during calorie restriction, beyond what can be explained by reduced mass of muscles, organs and fat.

Adaptive thermogenesis is seen when people continuously restrict calories by dieting and/or exercising. It may also be caused by weight loss drugs or surgery.

Although adaptive thermogenesis is well-known, how it works remains unclear.

STARVATION MODE: WHEN YOU EAT LESS, YOUR BODY BURNS LESS

ARTICLE REVIEWED

German researchers set out to investigate the causes and dynamics of adaptive thermogenesis (starvation mode).

They wanted to find out how body composition affects adaptive thermogenesis, whether it causes changes in hormones, and what effect it has on weight regain.

Muller et al. Metabolic Adaptation to Caloric Restriction and Subsequent Re-feeding: The Minnesota Starvation Experiment Revisited. American Journal of Clinical Nutrition 2015.

STUDY DESIGN

The article describes the results of two related studies from Christian Albrechts University, in Germany.

The design was similar to the famous Minnesota Starvation Experiment from 1950, one of the most important early studies on the effects of starvation in humans (4).

STUDY 1

This 6-week intervention study included 32 healthy, non-obese men, between 20 and 37 years of age.

Before the intervention started, participants spent 10 weeks at the university’s metabolic ward where their energy needs were calculated.

The intervention was divided into three parts:

  1. Overfeeding: For one week, the participants were overfed so that their calorie intake exceeded their energy needs by 50%.
  2. Calorie restriction: For three weeks, the participants were semi-starved so that their calorie intake was 50% lower than their energy needs.
  3. Re-feeding: For two weeks, the participants were again overfed so that their calorie intake exceeded their needs by 50%.

All participants spent every day, from 8 AM to 6 PM, at the university’s metabolic ward, where they were measured and monitored.

Dietary intake was strictly controlled. All foods were weighed and all meals supervised.

Additionally, participants were encouraged to avoid any physical activity and to remain sedentary.

Compliance was ensured by using continuous 24-h glucose monitors, pedometers and dietary records.

Body composition was measured using various techniques. These included quantitative magnetic resonance and whole-body MRI.

The levels of various hormones and other relevant body processes were also analyzed throughout the study.

 

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STUDY 2

A smaller follow-up study was done 1.5 years later than the original study.

This study included only eight of the participants that took part in the first study.

Its purpose was to estimate the effects of short-term calorie restriction on adaptive thermogenesis.

Additionally, it examined whether the results of the earlier study were reproducible.

It was divided into two parts:

  1. Overfeeding: Participants were overfed for one week.
  2. Calorie restriction: Participants were calorie restricted for one week.

Otherwise, the methods were similar to the first study.

 

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RESULTS

This chart below shows the changes in body composition over the course of the study (click to enlarge):

The top graph shows change in body weight, the middle graph shows a change in fat mass, and the bottom graph shows nitrogen balance, which indicates changes in lean mass (mostly muscles and organs).

After three weeks of calorie restriction, body weight decreased by 6 kg (13.2 lbs – 7.5%) and resting energy expenditure dropped by 266 calories per day, on average.

Adaptive thermogenesis was detected in 60% of participants in the early stages of calorie restriction. It became significant on the third day.

It was partly responsible for the decrease in energy expenditure, accounting for 108 calories/day.

Of these 108 calories per day, 36 were explained by changes in the composition of fat-free mass, leaving 72 calories for “true” adaptive thermogenesis.

Factors that were associated with adaptive thermogenesis included reduced insulin levels, heart rate, kidney function and body fluid balance. Increased formation of glucose in the liver also appeared to play a role.

Adaptive thermogenesis was not associated with changes in sympathetic nervous system activity, total body fat, belly fat, liver fat, organ mass, nitrogen and sodium balances.

It was also not linked to hormonal changes, such as in leptin, ghrelin, adiponectin and thyroid hormone levels (T3).

Lastly, adaptive thermogenesis appears to have no long-term effects on weight or fat regain after short-term calorie restriction. The effect was reversed within two weeks of re-feeding.

Here you can see how energy expenditure changes from adaptive thermogenesis developed during the course of the study:

As you can see, the increase during the re-feeding phase completely reversed the decrease seen during the calorie restriction phase.

Several other parameters changed significantly during 3 weeks of severe calorie restriction:

  • Fat mass: Decreased by 114 grams per day.
  • Lean mass: Decreased by 159 grams per day (muscles and organs combined, see below).
  • Muscle mass: Decreased by 5%.
  • Liver mass: Decreased by 13%.
  • Kidney mass: Decreased by 8%.
  • Heart rate: Went down by 14%.
  • Blood pressure: Went down by 7%.
  • Creatinine clearance: Went down by 12%.
  • Energy cost of walking: Decreased by 22%.
  • Sympathetic nervous system activity: Decreased by 38%.
  • Leptin levels: Decreased by 44%.
  • Insulin levels: Decreased by 54%.
  • Adiponectin levels: Decreased by 49%.
  • Triiodothyronine (T3): Decreased by 39%.
  • Testosterone: Decreased by 11%.

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MAIN CONCLUSIONS

The main conclusions of the study were as follows:

  • Adaptive thermogenesis is modest and kicks in during the early stages of starvation, shortly after calorie restriction starts. It is maintained as long as you keep restricting calories.
  • Adaptive thermogenesis appears to have no long-term effects on weight or fat regain after short-term calorie restriction.
  • Adaptive thermogenesis was partially explained by reductions in heart rate and kidney function, and increased formation of glucose in the liver.
  • In early calorie restriction, adaptive thermogenesis is also associated with a drop in insulin levels.

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LIMITATIONS

The study has no apparent limitations. It was tightly controlled and had highly significant results.

However, since the participants were limited to healthy, sedentary, non-obese men, the results may not be generalized to all people.

For example, it is possible that the dynamics of of adaptive thermogenesis are vastly different in people with obesity.

WHAT DO OTHER STUDIES SAY?

In general, adaptive thermogenesis (AT) is considered to be an automatic response to food shortage.

In the Minnesota Starvation Experiment from 1950, resting energy expenditure declined by 39% (600 calories/day). About 35% of this decline was not caused by changes in body composition, which indicates that AT also played a role.

Additionally, studies in obese patients have detected adaptive thermogenesis amounting to 504 calories/day.

Reduced levels of leptin and thyroid hormone (T3) have often been considered as major determinants of AT.

Although the current study showed reductions in both leptin and T3, it did not support a causal relationship between AT and changes in these hormones.

This is supported by studies on obese patients after weight loss. They found no significant associations between AT and reductions in leptin and T3.

Some studies indicate that AT may contribute to increased weight regain after calorie restriction.

This effect has been referred to as the “fat overshooting” phenomenon.

According to the current study, this effect is reversed within 2 weeks of re-feeding.

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SUMMARY AND REAL-LIFE APPLICATION

In short, adaptive thermogenesis (AT) is one of the main reasons your body starts burning fewer calories when you lose weight.

It is a part of the reason why weight loss tends to slow down over time, and is often referred to as “starvation mode.

In the current study, significant adaptive thermogenesis was detected as early as on the third day of calorie restriction.

Unfortunately, there is no known way to completely prevent this from happening.

However, two effective ways to partly reduce muscle loss and metabolic slowdown during weight loss include strength training and keeping your protein intake high.

Additionally, by exercising more and staying active throughout the day, you can negate some of the reduction in energy expenditure.

Which Omega 3 oils are best – DHA is Better than EPA at Reducing Inflammation

DHA and EPA are long-chain omega-3 fatty acids that are well known for their health benefits.

Both are found in fatty fish, as well as fish oil supplements. Most research has examined their combined health effects, but few studies have compared them.

Recently, a large Canadian study compared the effects of DHA and EPA on inflammatory markers and blood lipids.

Here is a detailed summary of its findings.

Plant And Animal Sources Of Omega 3 Fatty Acids

Background

Many scientists believe that chronic, low-grade inflammation is a key factor in the development of lifestyle diseases, such as heart disease (12).

Several unhealthy lifestyle habits contribute to inflammation. One of them is the excessive consumption of omega-6 oils, relative to omega-3.

Excessive omega-6 intake is a consequence of the modern, processed diet. If you eat a lot of processed food and vegetable oils — mainly soybean, sunflower or corn oil — you are almost certainly getting too much omega-6.

Unlike omega-6, long-chain omega-3 fats are anti-inflammatory. There are two main types of long-chain omega-3 fats (34):

  • Eicosapentaenoic acid (EPA)
  • Docosahexaenoic acid (DHA)

Both EPA and DHA are found in seafood, fatty fish, fish oil and certain types of marine microalgae.

The body can also produce them from alpha-linolenic acid (ALA), which is found in many plant oils. However, the conversion of ALA to EPA and DHA is inefficient. It’s best to get EPA and DHA from your diet or supplements, rather than relying on ALA.

Few studies have compared the anti-inflammatory potential of EPA and DHA. Most have investigated mixtures of EPA and DHA or included only one of them (4).

Some studies suggest that DHA may be more effective at improving the blood lipid profile, but little is known about their individual effects on inflammation (5).

Article Reviewed

This study compared the effects of EPA or DHA supplementation on inflammatory markers and blood lipids.

Randomized, crossover, head-to-head comparison of EPA and DHA supplementation to reduce inflammation markers in men and women: the Comparing EPA to DHA Study.

Study Design

This was a double-blind, randomized controlled trial examining the effects of supplementing with EPA or DHA on markers of inflammation in healthy men and women.

The study recruited 48 men and 106 women with abdominal obesity and low-grade chronic inflammation.

They were randomly assigned to three groups:

  • EPA: This group took three 1-gram capsules, providing a total of 2.7 grams of eicosapentaenoic acid (EPA) every day for 10 weeks.
  • DHA: This group took three 1-gram capsules, providing a total of 2.7 grams of decahexaenoic acid (DHA) every day for 10 weeks.
  • Control: This group took three 1-gram capsules, providing a total of 3 grams of corn oil every day for 10 weeks. Corn oil is rich in omega-6 but contains very low amounts of omega-3.

The study had a crossover design, which means that the participants were assigned to all three treatments in a random order. Each treatment period was separated by a 9-week washout period.

During the study, the participants were asked to exclude all major sources of omega-3 from their diet.

At the start and end of each study period, the researchers measured the following:

  • Inflammatory markers: C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-18 (IL-18) and adiponectin.
  • Blood lipids: Triglycerides, total cholesterol, HDL-cholesterol and apolipoprotein B (apoB). LDL-cholesterol was calculated using the Friedewald equation.

Bottom Line: This was a randomized controlled trial comparing the effects of the omega-3 fats DHA and EPA on inflammatory markers and blood lipids.

Finding 1: DHA Reduced Inflammation More Than EPA

Supplementing with DHA caused a significantly greater reduction in inflammatory markers than EPA.

Specifically, DHA and EPA supplementation had the following effects, compared to the control (corn oil):

  • Interleukin-18 (IL-18): -7.0% with DHA, while EPA had no significant effects.
  • Interleukin-6 (IL-6): -12.0% with DHA and -13.4% with EPA.
  • Tumor necrosis factor-α (TNF-α): -14.8% with DHA, but EPA had no effects.
  • C-reactive protein (CRP): -7.9% with DHA, while EPA had no significant effects.
  • Adiponectin (AN): +3.1% with DHA, while EPA had no significant effects.

These findings are presented in the charts below:

IL 18

Three previous trials have compared the effects of supplementing with DHA or EPA on inflammatory markers. Supplementing with EPA or DHA did not affect any inflammatory markers (678).

However, those studies recruited only 25 or fewer participants for each group and had far less statistical power than the present study.

Bottom Line: Supplementing with DHA had a stronger anti-inflammatory effect than EPA.

Finding 2: DHA Improved the Blood Lipid Profile More Than EPA

Supplementing with DHA improved the blood lipid profile more than supplementing with EPA.

Specifically, DHA and EPA supplementation had the following effects, compared to control (corn oil):

  • Triglycerides (TG): -13.3% with DHA and -11.9% with EPA.
  • Total cholesterol (TC): +3.8% with DHA, while EPA had no significant effects.
  • HDL-cholesterol (HDL-C): +7.6% with DHA, while EPA had no effects.
  • LDL-cholesterol (LDL-C): +6.9% with DHA and +2.2% with EPA. DHA had a stronger effect on LDL-cholesterol in men (+12.5%), compared to women (+4.4%).
  • Apolipoprotein B (apoB): +4.5 with DHA, but EPA had no significant effects.
  • Cholesterol to HDL-cholesterol ratio (TC:HDL-C): -2.5% with DHA, but EPA had no significant effects.

These findings are presented in the chart below:

TG TC HDL LDL APOB TCHDL

The results are consistent with the findings of a previous meta-analysis showing that supplementing with DHA leads to a greater decrease in triglycerides and greater increases in LDL and HDL-cholesterol, compared to EPA (5).

DHA supplementation led to changes in triglycerides, apoB and LDL-cholesterol, which may suggest an increase in LDL particle size (a good change). However, future studies are needed to confirm this finding using proper measurements.

Bottom Line: Supplementing with DHA had greater effects on blood lipids than EPA. These changes appeared beneficial.

Limitations

The study had an excellent design and few methodological issues. However, the authors pointed out some minor limitations.

Circulating levels of DHA and EPA weren’t measured at the beginning of each study period. For this reason, it is unclear if the washout between treatment periods was long enough to eliminate all effects from the previous treatment period.

However, the levels of blood lipids and inflammatory markers were similar at the start of each of the periods, indicating that there were no residual effects from the previous treatment period.

Summary and Real-Life Application

In short, supplementing with 2.7 grams of DHA for 10 weeks was more effective than a similar dose of EPA at decreasing markers of chronic inflammation and improving the blood lipid profile in men and women with excessive belly fat.

However, more research is needed before we can claim that DHA is healthier than EPA. In fact, a recent study concluded that EPA may have greater benefits when it comes to heart disease prevention (9).

For the time being, it may be best to eat fatty fish, which provides both DHA and EPA, or choose mixed long-chain omega-3 supplements.

Diet and Gut Microbiota in Inflammation and Disease

Emerging evidence links chronic intestinal inflammation with obesity and metabolic disorders like insulin resistance.

What’s more, this association seems to be affected by changes in the gut microbiota caused by diet.

Recently, a group of researchers summarized the available evidence in a review published in Cell Metabolism. Below is an overview of the review’s main points.

Article Reviewed

This article discusses the association of intestinal inflammation, obesity, metabolic syndrome, the gut microbiota and dietary factors.

The Intestinal Immune System in Obesity and Insulin Resistance.

What is Inflammation?

Inflammation is the immune system’s response to infection, injury or toxins. There are two types of inflammation: acute inflammation and chronic inflammation.

Acute inflammation

Acute inflammation starts immediately after an injury or infection.

Its purpose is to eliminate foreign substances or invaders, such as bacteria or viruses, as well as to remove dead or injured cells that are no longer functional.

Although it causes the swelling and redness associated with wounds and infections, it is an essential process that helps the body heal and protects it against further harm.

Chronic inflammation

Chronic inflammation lasts longer than acute inflammation. For this reason, it damages living tissue. This increases the risk of diseases like cancer, heart disease and type 2 diabetes.

Many conditions may lead to chronic inflammation, including infection, toxin exposure, autoimmune diseases, age, high blood sugar levels or an unhealthy diet.

Low-grade, chronic inflammation is an underlying condition in obesity, insulin resistance and many other conditions.

Bottom Line: There are two types of inflammation: acute and chronic. Acute inflammation is a beneficial process, while chronic inflammation is associated with obesity and metabolic diseases.

Obesity is Associated With Dysbiosis

Obesity and metabolic syndrome are associated with dysbiosis, a term that refers to an imbalance in the gut microbiota (1).

Some scientists even believe that dysbiosis plays a key role in the development of obesity.

This idea is supported by animal studies, showing that mice without any bacteria in their intestines had lower amounts of body fat, and did not become obese or insulin resistant when put on a high-fat diet.

However, when the intestines of these same mice were colonized by gut bacteria from normal mice, they started to gain fat and develop insulin resistance (23).

What’s more, intestinal bacteria from obese mice increased fat gain more than bacteria from lean mice (1).

Consistently, killing the intestinal bacteria of obese mice with an antibiotic treatment reduced body fat and improved insulin sensitivity (45).

However, obese people should not resort to taking antibiotics, as there are other, healthier approaches. Human studies have shown that weight loss may restore gut microbiota balance and improve metabolic health (67).

Bottom Line: Different types of bacteria are predominant in obese people’s guts. These bacteria make it easier for them to absorb calories and gain fat.

Dysbiosis May Cause Intestinal Inflammation

Studies indicate that obesity-associated dysbiosis may promote weight gain. This is because obese people may have greater numbers of bacteria that improve calorie absorption.

Dysbiosis also seems to be characterized by low numbers of beneficial, anti-inflammatory bacteria.

These bacteria feed on fiber, especially prebiotic fiber, and produce short-chain fatty acids like butyrate. Butyrate improves colon health and reduces inflammation.

For this reason, a lack of butyrate-producing bacteria may promote intestinal inflammation.

Transferring gut bacteria from lean, healthy donors to those with metabolic syndrome increased the butyrate-producing bacteria, which improved insulin sensitivity (8).

This also seems to be related to diet, in that obese people tend to have lower bacterial diversity and richness in their guts. However, one study showed that bacterial diversity can be restored by eating less (910).

Bottom Line: An imbalance in the microbiota of obese individuals may lead to intestinal inflammation. This imbalance is characterized by low numbers of beneficial, anti-inflammatory bacteria.

Dysbiosis May Weaken the Gut Wall

Intestinal permeability is an essential function of the gut wall. It allows nutrients to pass across the gut barrier into the blood circulation.

But the gut barrier should not be too permeable, since it needs to prevent potentially harmful substances from entering the body.

However, excessive intestinal permeability is an unfortunate consequence of dysbiosis and intestinal inflammation.

This leads to the leakage of bacteria or bacterial toxins across the gut barrier, worsening systemic inflammation and metabolic disease. This condition is called metabolic endotoxemia (41112).

Endotoxemia is associated with high calorie intake, high intake of saturated fat, abdominal obesity and an increased risk of diabetes (1314).

Conversely, getting enough fiber might help prevent endotoxemia by increasing the numbers of beneficial bacteria and strengthening the gut barrier (15).

Nevertheless, further studies are needed before any solid conclusions can be reached.

Bottom Line: Dysbiosis and intestinal inflammation may also increase intestinal permeability, allowing harmful substances to “leak” across the gut barrier. This may worsen inflammation and metabolic disorders.

Dietary Factors Affect Intestinal Inflammation

Intestinal inflammation is not only associated with dysbiosis and a “leaky gut.” All of this also appears to be linked to dietary habits.

Dietary factors that may worsen intestinal inflammation include:

  • A diet high in saturated fat: A diet high in saturated fat has been associated with intestinal inflammation in mice. This effect appears to be mediated by the gut microbiota, since bacteria-free mice showed no effects (161718).
  • Food emulsifiers: Another mouse study suggests that two commonly-used food emulsifiers may change the gut microbiota and worsen inflammation (19).

Other dietary factors may protect against inflammation:

  • Losing weight: One human study showed that losing weight reduced intestinal inflammation, while also improving blood sugar levels and blood lipids (20).
  • Omega-3 fatty acids: A study in mice found that saturated fats from lard increased inflammation, whereas polyunsaturated fats from fish oil protected against inflammation (16).
  • Probiotics: Several types of probiotic bacteria may reduce intestinal inflammation and strengthen the gut barrier (2122232425).
  • Antioxidants: Antioxidant polyphenols from fruits and vegetables may also reduce inflammation (26).
  • Prebiotic fiber: Eating plenty of prebiotic fiber encourages the growth of beneficial bacteria that produce anti-inflammatory short-chain fatty acids, such as butyrate (27).

Several studies have also examined the effects of anti-inflammatory drugs on intestinal inflammation and metabolic conditions.

Apart from reducing inflammation, anti-inflammatory drugs may improve insulin sensitivity, decrease fasting blood sugar, reduce endotoxemia and increase gut bacterial diversity, without any effects on body weight (282930).

Taken together, these findings support the idea that diet-induced inflammation plays a key role in the development of chronic diseases in obesity.

Bottom Line: Dietary factors may either worsen or improve intestinal inflammation. Many of these effects seem to be mediated by the gut microbiota.

Summary and Real-Life Application

Obesity and many metabolic disorders are associated with chronic intestinal inflammation. Dietary factors and the gut microbiota also play a key role.

Fortunately, dietary strategies may be able to prevent or reduce these problems. These strategies may also improve many obesity-related metabolic conditions, such as insulin resistance.

Effective strategies include losing weight, eating omega-3s, and taking prebiotic fiber and probiotics.

DASH Diet Lowers Inflammation and blood pressure


DASH stands for Dietary Approaches to Stop Hypertension.

The DASH diet is designed to reduce blood pressure and improve blood lipids.

It’s typically low in fat and relatively high in carbs, but it’s not clear what role these macronutrients play in the diet’s effectiveness.

For this reason, a group of researchers compared the effects of a higher-fat, lower-carb DASH diet to the conventional DASH diet.

Their results were recently published in the American Journal of Clinical Nutrition.

The DASH diet focuses on fruits, vegetables, whole grains and lean meats.

The diet was designed after researchers noticed that high blood pressure was much less common in those who followed a plant-based diet, such as vegans and vegetarians, than in meat eaters (56).

This led researchers to design a diet that provided liberal amounts of the nutrients that appeared to protect people against high blood pressure.

The result was the DASH diet, which is high in fruits and vegetables and contains some lean protein sources like chicken, fish and beans. The diet is low in red meat, salt, added sugars and fat.

It’s thought that one of the main reasons people with high blood pressure can benefit from this diet is because it reduces the amount of salt they’re eating.

The regular DASH diet program recommends that people eat no more than 2,300 mg of sodium per day (or 1 teaspoon), which is in line with most national guidelines.

The lower-salt version recommends that people eat no more than 1,500 mg of sodium per day (or 3/4 of a teaspoon).

Conclusion: The DASH diet was designed to reduce high blood pressure. It’s rich in fruits, vegetables and lean proteins, but it restricts red meat, salt, added sugars and fat.

Background

It is currently the world’s most popular diet aimed at lowering blood pressure and reducing the risk of heart disease.

The original DASH diet has the following characteristics (12):

  • High in fruits and vegetables.
  • High in whole grains and fiber.
  • Includes nuts, seeds and legumes several times weekly.
  • High in low-fat dairy products.
  • Relatively low in red meat, poultry and fish.
  • Low in saturated fat, cholesterol and sodium.
  • Relatively high in potassium, magnesium and calcium.
  • Relatively low in refined sugar.

A large, observational study, called the Nurses’ Health Study, found a DASH-type diet to be associated with a reduced risk of heart disease and stroke (3).

Some researchers believe that the DASH diet may reduce heart disease risk because of its low saturated fat content (45).

The DASH Diet Lowers Blood Pressure

Blood pressure is a measure of the force put on your blood vessels and organs as your blood passes through them. It’s counted in two numbers:

  • Systolic pressure: The pressure in your blood vessels when your heart beats.
  • Diastolic pressure: The pressure in your blood vessels between heartbeats, when your heart is at rest.

Normal blood pressure for adults is a systolic pressure below 120 mmHg and a diastolic pressure below 80 mmHg. This is normally written with the systolic pressure written above the diastolic pressure, like this: 120/80.

People with a blood pressure reading of 140/90 are considered to have high blood pressure.

Interestingly, the DASH diet has been shown to lower blood pressure in both healthy people and those who already have high blood pressure.

Furthermore, it achieved this even though people didn’t lose weight or restrict their salt intake (78).

However, when sodium intake was restricted, they found that the DASH diet lowered blood pressure even further. In fact, the greatest reductions in blood pressure were seen in people with the lowest intakes of salt (9).

These low-salt DASH diet results were most impressive in people who already had high blood pressure, reducing it by an average of 11 points. In people with normal blood pressure, it reduced blood pressure by three points (5).

This is in line with other studies that have found that restricting salt intake can reduce blood pressure, especially in those who have high blood pressure (10).

However, it’s important to note that a decrease in blood pressure does not always translate to a decreased risk of heart disease or death (11).

Conclusion: Following a DASH dietary pattern is effective at lowering blood pressure, especially in people who already have high blood pressure.

Can You Lose Weight on the DASH Diet?

Apples, Grapes, a Fork and a Knife on Scales

The DASH diet has been shown to reduce blood pressure, regardless of whether people lose weight or not.

However, if you already have high blood pressure, chances are you have been advised to lose weight.

This is because the more you weigh, the higher your blood pressure is likely to be (121314).

Additionally, losing weight has been shown to lower blood pressure (1516).

Some studies have shown that people can lose weight on the DASH diet (171819).

However, those who have lost weight on the DASH diet have been in a controlled calorie deficit, meaning they were told to eat fewer calories than they were using.

Given that the DASH diet cuts out lots of high-fat, sugary foods, people may find that they automatically reduce their calorie intake and lose weight. Other people may have to consciously restrict their intake (20).

Either way, if you want to lose weight on the DASH diet, you’ll still need to reduce your calorie intake so you’re taking in fewer calories than you are using up.

Conclusion: The DASH diet could help you lose weight. However, for weight loss to occur, you still have to make sure you’re eating fewer calories than you’re burning.

Other Potential Health Benefits

Salmon and Vegetables

It’s well documented that the DASH diet can help lower blood pressure. However, the diet has additional benefits.

Here are some recorded benefits of the DASH diet:

  • Decreases cancer risk: A recent review found that people following the DASH diet had a lower risk of some cancers, including colorectal and breast cancer (21).
  • Lowers metabolic syndrome risk: Some studies have shown that the DASH diet reduces your risk of developing metabolic syndrome by up to 81% (2223).
  • Lowers diabetes risk: Following the DASH diet has been linked to a lower risk of developing type 2 diabetes. Some studies have also shown that it can improve insulin resistance (2425).
  • Decreases heart disease risk: One recent review showed that in women, following a DASH-like diet was associated with a 20% lower risk of heart disease and a 29% lower risk of stroke (26).

Many of these protective effects have been attributed to the high fruit and vegetable content of the DASH diet. This is because, in general, eating more fruits and vegetables is linked to a reduced risk of disease (27282930).

Conclusion: A DASH dietary pattern could reduce your risk of some cancers, diabetes, heart disease and metabolic syndrome.

Does the DASH Diet Work for Everyone?

One of the key findings of DASH diet studies was that the greatest reductions in blood pressure were seen in those with the lowest intakes of salt.

While this is interesting, the benefits of salt restriction on health and lifespan are not clear cut. For people with high blood pressure, reducing salt intake has been shown to significantly affect blood pressure (6).

However, in people who have normal blood pressure, the effects of reducing salt intake are much smaller (10).

This could partly be explained by the theory that some people are “salt sensitive,” meaning some people are more sensitive to salt and that it has a greater effect on their blood pressure (31).

Conclusion: Lowering salt intake from very high levels is beneficial for most people. Further salt restriction, as advised on the DASH diet, may only be beneficial for people who are “salt sensitive” and have high blood pressure.

 

DASH Diet Foods Plus Dairy

Article Reviewed

A team of scientists from the Children’s Hospital Oakland Research Institute, in California, compared the effects of the standard DASH diet and a higher-fat, lower-carb DASH diet on blood pressure and blood lipids.

Comparison of the DASH (Dietary Approaches to Stop Hypertension) diet and a higher-fat DASH diet on blood pressure and lipids and lipoproteins: a randomized controlled trial.

Basic Study Design

This randomized, controlled trial examined the effects of a modified DASH diet and the standard DASH diet on blood pressure and blood lipids. The modified diet included more dairy fat and fewer carbs.

The participants were healthy men and women with systolic blood pressure less than 160 mm Hg, and diastolic blood pressure between 80 and 95 mm Hg.

The participants were assigned to three groups in random order:

  • Standard DASH diet: Participants followed the conventional DASH diet.
  • Higher-fat DASH diet: This diet included more dairy fat and less carbs, but was otherwise identical to the standard DASH diet.
  • Control diet: The control diet was designed to represent a normal Western diet.

In the higher-fat DASH diet, the saturated fat content was increased from 8% to 14% of daily calories. To keep the calorie content the same, the carb content was also reduced by 12% of daily calories.

Each of these diets lasted for 3 weeks. The study had a crossover design, meaning that all of the participants followed all three diets during different study periods, separated by a 2-week washout period.

At the beginning and end of each of the three diets, the researchers measured blood pressure, blood lipids, body weight and body fat.

A total of 36 participants completed the study.

Conclusion: This randomized, crossover trial examined the effects of a higher-fat, lower-carb DASH diet on blood pressure and blood lipids.

Finding 1: Dairy Fat Did Not Adversely Affect Blood Pressure

Both the standard DASH diet and the higher-fat DASH diet reduced blood pressure to a similar extent, compared to the control diet, as shown in the chart below.

DASH Diets and Control Blood Pressure

However, blood pressure was significantly lower two weeks after the participants had finished the higher-fat DASH diet, suggesting delayed effects.

This means that eating more saturated dairy fat on the DASH diet does not adversely affect blood pressure.

Other studies have found that modifying the standard DASH diet by replacing carbs with unsaturated fat or protein yields similar or greater improvements in blood pressure (678).

Conclusion: The standard DASH diet and the higher-fat DASH diet reduced blood pressure to a similar extent, compared to the control diet.

Finding 2: Higher-Fat DASH Diet Reduced Triglycerides

The DASH diet and the higher-fat DASH diet had different effects on the blood lipid profile. The higher-fat DASH diet reduced the levels of triglycerides, as shown in the chart below.

DASH Diets and Control Triglycerides

This modest reduction in triglycerides may be explained by the lower amounts of carbs in the higher-fat DASH diet, compared to the standard DASH diet (9).

Conclusion: The higher-fat DASH diet reduced triglycerides, compared to the standard DASH diet, due to the lower carb content of the higher-fat diet.

Finding 3: Effects on LDL Peak Diameter

High levels of small, low-density lipoproteins (LDL) have been associated with an increased risk of heart disease (10).

In the present study, the conventional DASH diet reduced the peak diameter of the LDL particles, but the higher-fat DASH diet increased the peak diameter, compared to the control diet.

DASH Diets and Control LDL Peak

This means that the higher-fat DASH diet may have caused a modest increase in LDL particle size.

In fact, there was a trend for higher levels of large LDL particles with the higher-fat DASH diet, but the findings were not significant.

Previous studies have shown that reduced carb and sugar intake may cause a shift from smaller to larger LDL particles, explaining the present findings (1112).

Conclusion: The higher-fat DASH diet increased LDL peak diameter, whereas the standard DASH reduced the LDL peak diameter. Large LDL size has been associated with a reduced risk of heart disease.

Finding 4: No Increase in LDL-Cholesterol

The higher-fat DASH diet did not increase levels of LDL-cholesterol, compared to the standard DASH diet.

This is inconsistent with studies showing that replacing carbs or unsaturated fats with saturated fats increases LDL-cholesterol (913).

The authors speculate that the DASH diet may have characteristics that prevent the rise in LDL-cholesterol typically associated with a higher intake of saturated fats.

Conclusion: The higher-fat DASH diet did not increase LDL-cholesterol, compared to the standard DASH.

Limitations

This study appears to have been designed and implemented well.

It was a crossover trial, meaning that all participants were on all three diets during different study periods, separated by a 2-week washout period.

The purpose of the washout period was to prevent the previous diet from affecting the results of the next diet.

This washout, however, doesn’t appear to have worked in all cases, since there were some prolonged effects of the higher-fat DASH diet on blood pressure. The reason for this is unexplained.

Other limitations include a small number of participants and a relatively short study period.

Conclusion: This study did not have any serious limitations. However, the 2-week washout period between diets may not have been long enough with respect to blood pressure.

How to Make Your Diet More DASH-Like

Because there are no set foods on the DASH diet, you can adapt your current diet to the DASH guidelines by doing the following:

  • Eat more vegetables and fruits.
  • Swap refined grains for whole grains.
  • Choose fat-free or low-fat dairy products.
  • Choose lean protein sources like fish, poultry and beans.
  • Cook with vegetable oils.
  • Limit your intake of foods high in added sugars, like soda and candy.
  • Limit your intake of foods high in saturated fats like fatty meats, full-fat dairy and oils like coconut and palm oil.

Outside of measured fresh fruit juice portions, this diet recommends you stick to low-calorie drinks like water, tea and coffee.

Conclusion: It’s possible to adapt your current diet to align with the DASH diet. Simply eat more fruits and vegetables, choose low-fat products and lean proteins and limit your intake of processed, high-fat and sugary foods.

Frequently Asked Questions

If you’re thinking about trying the DASH approach for your blood pressure, then you might have a few questions about other aspects of your lifestyle.

The most commonly asked questions are addressed below.

Can I Drink Coffee on the DASH Diet?

Coffee in a Blue Cup

The DASH diet doesn’t prescribe specific guidelines for coffee. However, some people worry that caffeinated beverages like coffee may increase their blood pressure.

It’s well known that caffeine can cause a short-term increase in blood pressure (33).

Furthermore, this rise is greater in people with high blood pressure (3435).

However, a recent review found that despite coffee causing a short-term (1–3 hours) increase in blood pressure, it didn’t increase the long-term risk of high blood pressure or heart disease (33).

For most healthy people with normal blood pressure, 3–4 regular coffees per day are considered safe (36).

However, the slight rise in blood pressure (5–10 mm Hg) caused by caffeine means that people who already have high blood pressure probably need to be more careful with their coffee consumption.

Do I Need to Exercise on the DASH Diet?

The DASH diet has been shown to be even more effective at lowering blood pressure when people are also active (18).

Given the independent benefits of exercise on health, this is not surprising.

It’s recommended to do 30 minutes of moderate activity most days, and it’s important to choose something you enjoy, as you will be more likely to keep it up.

Examples of moderate activity include:

  • Walking (15 min/mile)
  • Running (10 min/mile)
  • Cycling (6 min/mile)
  • Swimming laps (20 mins)
  • Housework (60 mins)

Can I Drink Alcohol on the DASH Diet?

Glass of Red Wine

Drinking too much alcohol can increase your blood pressure (37).

In fact, regularly drinking more than three drinks per day has been linked to an increased risk of high blood pressure and heart disease (38).

On the DASH diet, it’s recommended that you drink alcohol sparingly and don’t exceed the national government guidelines — two or fewer drinks per day for men and one or fewer drinks per day for women.

: You can drink coffee and alcohol in moderation on the DASH diet. Combining the DASH diet with exercise may make it even more effective.

Summary and Real-Life Application

In short, this study shows that eating slightly more saturated dairy fat while on the DASH diet does not affect its beneficial effects on blood pressure.

Also, it did not have any adverse effects on the blood lipid profile.

A lower-carb, higher-fat DASH diet is a healthy, equally effective option, which may be easier to follow than the standard DASH diet.

For some people, the DASH diet may be easy to stick to and an effective way to reduce blood pressure.

However, it’s worth noting that reducing salt intake to 1,500 mg or less has not been linked to any hard health benefits, such as a reduced risk of heart disease or death, despite the fact that it can lower blood pressure.

Moreover, the DASH diet is very similar to the standard low-fat diet, which large controlled trials have not shown to reduce the risk of death (3940).