5 Day Fast – Using the Fast Mimicking Diet

Recently I began a 3-day fast, which then got extended to 5 days.

The intention was to use the “Tim Ferriss method” (described here). Essentially accelerating the shift from glucose burning to fat burning as quick as possible, avoiding the negative physical feelings associated with the transition period. (60 second video primer on ketones if you’re not familiar).

However, in the process of researching more about the measurement of blood glucose and blood ketones, I realised its possible to experiment a bit.

There has been some excellent research done by Valter Longo and his colleagues at the University of Southern California on a way to do fasts, without completely stopping eating.

Essentially, they were aware of all the health benefits associated with fasting, but wanted to tackle the problem of compliance. For most people these days, the thought of not eating for 5 days is too much to handle.

They have come up with a 5 day diet that is low enough in calories and carbohydrates, that the user gets the vast majority of the benefits from fasting.

Actually, they have patented their specific diet as prolonfmd.com – and are selling it to hospitals to prescribe to their patients. Your first thought is probably…huh? But its more about “playing the game”, and finding ways to get fasting into hospitals, than it is about money. I believe Valter has even gone as far as to pledge his profits from the endeavour to charity. For more on Valter Longo and the FMD diet – check out Rhonda Patrick’s podcast with him.

What patients would find when they use the prescription Prolon diet

Luckily for us, we can use Valter’s research into fasting, without getting a prescription for his diet. In the paper that they published to cell.com, they describe the details of the diet:

The human FMD diet consists of a 5 day regimen:
– Day 1 of the diet supplies 1,090 kcal (10% protein, 56% fat, 34% carbohydrate)
– Days 2–5 are identical in formulation and provide 725 kcal (9% protein, 44% fat, 47% carbohydrate).

Damien, of Quantified Body figured out that this is similar to the macronutrient composition of avocados. So for example, you could have 2 medium sized avocados per day on each of the 5 days.

It doesn’t have to be avocados though, it could be anything that fits the above macros.

The other interesting piece of the puzzle, that contributed to this fast, was a paper by Dr Seyfried on treating brain cancer.

They found that if they could keep patients in what they termed “nutritional ketosis”, then they could achieve remission in some patients. Nutritional ketosis differs from simply measuring blood ketone levels, instead it measures the ratio between blood glucose and blood ketones. I’ve written in more detail here about it.

The sweet spot where blood glucose drops and blood ketones rise. This graph comes from Seyfried’s experiment to halt tumor growth.

My 5 Day Fast Details

The crux of my experiment, is that adding in some calories/nutrition makes the whole process MUCH easier. And you can do it in a calculated way.

Here’s the rough breakdown of what I consumed:

  • Day 1 (after 24h) – 2 tablespoons of MCT oil (C8)
  • Day 2 – 2 tablespoons of MCT oil (C8) + 1 tablespoon of coconut oil
  • Day 3 – 1 avocado (with Himalayan sea salt + apple cider vinegar) + 1 tablespoon of coconut oil
  • Day 4 – 2 avocados (again with Himalayan sea and apple cider vinegar) + 1 tablespoon of coconut oil + 1 tablespoon of MCT oil (C8)
  • Day 5 – Nothing until I broke the fast in the evening

You can see I didn’t adhere strictly to the fast mimicking diet, and was generally under the prescribed amount of calories. But was far in excess of a simple water fast.

From the end of day 1, my ketones were elevated (no doubt helped by the MCT oil). Highest they reached was about 4.4mmol/L, with blood glucose simultaneously at 2.8mmol/L.

2.8 mmol/L blood glucose reading (about 39 mg/dL)


4.4 mmol/L blood ketone

The measurement of blood ketones and blood glucose come in useful for 3 main things:

  1. Tracking your transition into ketosis – and correlating how you feel with where you are in ketosis
  2. Giving you a measurable goal to aim for and maintain! (this is huge)
  3. You can use the blood measurements to test how different foods / ketone sources affect them

Regarding #3 – when I ate the second avocado on day 3, my bloods actually showed I came out of nutritional ketosis. Even though my ketones were at 2.5 mmol/L, my blood glucose was at 4.3 mmol/L. Which is a ratio of 1.72 – rather than the desired ratio of 1.0 or lower.

After Thoughts

All in all this experiment was a success.

Its becoming increasingly more obvious that fasting is an important tool in humanities arsenal against disease. Once upon a time, as hunter and gatherers, these fasted states were forced on us by the environment. Now in today’s abundant first world, we have to artificially create them. As with any “medicine”, one of the big hurdles is compliance.

The last 5 day fast I did was back in November, and it was taxing to say the least. I certainly didn’t feel in a rush to do another one. However, this time around, I felt much more functional throughout the fast – and can see a way to make this a more regular thing. Regular being something in the order of twice per year.

Exiting The Fast + Ketosis

Probably the worst part of the fast this time was the exit. I think it comes down to the harsh way I went from nutritional ketosis, to consuming reasonably high levels of carbohydrates. In retrospect, I’d probably prepare a meal with some fatty meat + vegetables. That way it fulfils the need I have to *eat everything*, but won’t cause such a harsh crash after.

I’ve never been a strong believer in living in ketosis, and I’m still not. But there’s something about seeing the effect on your body when it goes from ketosis to glucose burning, that makes you question if you’re doing it a favour!

Further Questions

There’s a few points from this experiment I’d like to learn more about:

  • Evening of day 3 I was still producing ketones, but out of nutritional ketosis. Morning of day 4 I was back in nutritional ketosis. What effect does coming out of nutritional ketosis have on the overall efficacy of the fast?
  • If we were to compare a completely water based fast, to the fast mimicking diet, what are we losing out on?
  • If we are losing out on something, could this be mitigated by going to 6 or 7 days?

Anyway, that’s a rather large brain dump. Hopefully if you’ve got this far you’ve been able to extract some nuggets to help you in your journey. If you’ve got any questions or comments, please leave them below. As for any blogger, feedback is wonderful.

Keto Diet better than high carb for Type 2 diabetes

Type 2 diabetes is a common condition characterized by high levels of blood sugar, usually due to insulin resistance.

The treatment of type 2 diabetes involves medication, but lifestyle strategies are very important as well.

These include increased exercise, weight loss and diet management.

Although low-carb diets have become popular for managing type 2 diabetes, few high-quality studies have investigated their long-term effects on blood sugar control and risk factors for heart disease.

Low-Carb diets


A team of Australian researchers set out to compare the long-term health effects of a low-carb diet and a high-carb diet, focusing on differences in blood sugar control and risk factors for heart disease.

Tay et al. Comparison of Low- and High-Carbohydrate Diets for Type 2 Diabetes Management: A Randomized Trial. American Journal of Clinical Nutrition 2015.


This was a randomized trial that spanned one year, or 52 weeks total.

A total of 115 obese and overweight adults with type 2 diabetes participated. Their age ranged from 35 to 68 years.

The participants were randomly assigned to one of two diets that contained an equal amount of calories:

  • Low-carb diet (LC): Carbs, protein and fat comprised 14%, 28% and 58% of calories, respectively. The total carb content was under 50 grams per day.
  • High-carb diet (HC): Carbs, protein and fat comprised 53%, 17% and 30% of calories, respectively.

Both diets restricted calories in order to produce weight loss. Calories were restricted by 30%, which amounted to 500–1000 calories, depending on the individual.

The fat content of the diets was mainly unsaturated, with less than 10% of calories from saturated fats.

In addition, all participants had 60-minute, supervised exercise sessions three times per week. These sessions focused on moderate-intensity aerobic and resistance exercise.

Blood samples were taken at the beginning, in the middle (24 weeks), and at the end (52 weeks) of the study.


78 people completed the study, which is 68% of participants.

Due to regular exercise and the reduction of calories, participants in both groups lost weight and achieved significant health improvements.

This graph shows the weight changes in the two groups:


Changes in the following health markers were similar between groups:

  • Weight loss: The LC group lost 9.8 kg (21.6 lbs) and the HC group lost 10.1 kg (22.3 lbs).
  • HbA1c: Levels dropped by 1% in both groups.
  • Fasting blood sugar: Decreased by 0.7 mmol/L (27.02 mg/dL) in the LC group and 1.5 mmol/L (57.9 mg/dL) in the HC group.
  • LDL cholesterol: Levels dropped by 0.1 mmol/L (3.9 mg/dL) in the LC group and 0.2 mmol/L (7.7 mg/dL) in the HC group.
  • Blood pressure: Fell by 7.1 mmHg in the LC group and 5.8 mmHg in the HC group.
  • Inflammation: Estimated by the C-reactive protein, this decreased by 0.9 mg/L in the LC group and 1.2 mg/L in the HC group.
  • Insulin resistance: Also decreased substantially.

However, the low-carb group experienced significantly greater improvements in several health markers.

These included improvements in the following:

  • Medication: Greater reduction in the need for diabetes medication.
  • Glycemic variability: At least twice the decrease in glycemic variability, indicating greater stability in blood sugar levels.
  • Hyperglycemia: Less risk of experiencing high blood sugar levels.
  • Triglycerides: 0.4 mmol/L (7.2 mg/dl) reduction in triglycerides, versus a 0.01 mmol/L (0.18 mg/dl) reduction in the HC group.
  • HDL cholesterol: Increases of 0.1 mmol/L (1.8 mg/dl), versus 0.06 mmol/L (1.08 mg/dl) in the HC group.


For overweight or obese people with type 2 diabetes, calorie-restricted diets and regular exercise lead to weight loss, improved blood sugar control and reduced risk factors for heart disease.

This happens regardless of whether people follow low-carb or high-carb diets.

However, low-carb diets lead to greater improvements in blood sugar control and blood lipid profile than high-carb diets.

Additionally, low-carb diets decrease the need for diabetes medication and help stabilize blood sugar levels.

For this reason, low-carb diets can help effectively manage type 2 diabetes.


This study was well designed, but had a few limitations.

  1. It did not include a control group of participants who did not change their diet, which would have helped isolate the effects of the lifestyle modifications.
  2. The assignment to diets was not blind.
  3. The LC group’s protein intake was much higher. Protein can affect weight loss as well as glycemic control, so this may have impacted the results of the study.
  4. By the end of the study, the LC group had increased their carbohydrate intake to 74 g, and saturated fat accounted for 11% of calories. Calorie intake was increased throughout the study in both groups.
  5. Adherence to the diet was good but not perfect, which is a common limitation of these types of studies.



The main outcome variable of the current study was HbA1c.

HbA1c is also known as glycated hemoglobin. Measuring HbA1c gives clinicians and scientists an idea of the average blood sugar levels over the previous few months.

High HbA1c levels are associated with an increased risk of developing diabetes-related complications.

Some studies have found no significant differences in the effects of low- and high-carb diets on HbA1c. Conversely, other studies have reported greater reductions in HbA1c with LC diets.


Studies that have compared LC diets with calorie-restricted HC diets among patients with type 2 diabetes have provided mixed results.

Some reported that LC diets caused greater weight loss.

In the current study, both diets contained the same amount of calories, and weight loss was similar.

This suggests that the main cause of weight loss is calorie deficit rather than the nutrient composition of the diets. Several previous studies support this.


Supporting the present study, one 24-week randomized controlled trial in obese adults with type 2 diabetes showed that a LC diet caused greater improvements in blood sugar control and blood lipid profile than a HC diet.

Similarly, previous studies have reported greater reductions in triglycerides and higher increases in HDL-cholesterol with LC diets.

In the current study, similar reductions in LDL-cholesterol were seen in both the LC and HC diets.

In contrast, large reviews of previous trials suggest that very LC diets may have less favorable effects on LDL cholesterol than conventional high-carb, low-fat diets.

These differences may be explained by the type of fat replacing carbs in LC diets. In the present study, carbs were replaced with unsaturated fat, which may lower LDL-cholesterol.

Conversely, saturated fats may raise the levels of LDL-cholesterol.


In conclusion, reducing calories and increasing exercise can lead to weight loss and improved health — regardless of whether people are on a low-carb or high-carb diet.

However, for obese people who have type 2 diabetes, a low-carb diet seems to be more effective at improving blood sugar control and reducing the risk factors for heart disease.

This is supported by several studies showing that low-carb diets are effective for diabetics.

Proof that Ketogenic Diets Increase NAD+ to Curb Inflammation and prevent brain degeneration


Ketogenic diets — extreme low-carbohydrate, high-fat regimens that have long been known to benefit epilepsy and other neurological illnesses — may work by lowering inflammation in the brain, according to new research by UC San Francisco scientists. The UCSF team has discovered a molecular key to the diet’s apparent effects, opening the door for new therapies that could reduce harmful brain inflammation following stroke and brain trauma by mimicking the beneficial effects of an extreme low-carb diet

New research uncovers and replicates the mechanism by which a ketogenic diet curbs brain inflammation. The findings pave the way for a new drug target that could achieve the same benefits of a keto diet without having to actually follow one.

The keto diet is focused on reducing the amount of carbohydrates as much as possible and increasing the amount of protein and fat.

Besides its weight loss-related benefits, recent studies have pointied to many other advantages. For instance, Medical News Today recently covered research suggesting that the diet may increase longevity and improve memory in old age.

Other studies have noted the neurological benefits of the diet. The keto diet is used to treat epilepsy, and some have suggested that it may prove helpful in Alzheimer’s and Parkinson’s disease.

However, the mechanism by which a keto diet may benefit the brain in these illnesses has been a mystery. The new research – which was led by Dr. Raymond Swanson, a professor of neurology at the University of California, San Francisco – suggests that it may do so by reducing brain inflammation.

In the new study, Dr. Swanson and team show the molecular process by which the keto diet reduces brain inflammation. The researchers also identify a key protein that, if blocked, could create the effects of a keto diet.

This means that a drug could be designed to reduce inflammation in patients who cannot follow a keto diet because of other health reasons.

The findings were published in the journal Nature Communications.

A keto state lowers brain inflammation

A keto diet changes the metabolism, or the way in which the body processes energy. In a keto diet, the body is deprived of glucose derived from carbs, so it starts using fat as an alternative source of energy.

In the new study, Dr. Swanson and his colleagues recreated this effect by using a molecule called 2-deoxyglucose (2DG).

The 2DG molecule stopped glucose from metabolizing and created a ketogenic state in rodents with brain inflammation as well as in cell cultures. Levels of inflammation were drastically reduced – almost to healthy levels – as a result.

“We were surprised by the magnitude of our findings,” said Dr. Swanson. “Inflammation is controlled by many different factors, so we were surprised to see such a large effect by manipulating this one factor. It reinforces the powerful effect of diet on inflammation.”

The restricted glucose metabolism lowered the so-called NADH/NAD+ ratio. Dr. Swanson explained to MNT what this ratio refers to, saying, “NAD+ and NADH are naturally occurring molecules in cells that are involved in energy metabolism.”

“Cells convert NAD+ to NADH, as an intermediary step in generating energy from glucose, and thus increase the NADH/NAD+ ratio,” he added.

When this ratio is lowered, the CtBP protein gets activated and attempts to turn off inflammatory genes. As Dr. Swanson told us, “CtBP is a protein that senses the NADH/NAD ratio and regulates gene expression depending on this ratio.”

So, the scientists designed a molecule that stops CtBP from being inactive. This keeps the protein in a constant “watchful” state, blocking inflammatory genes in an imitation of the ketogenic state.

Significance of the findings, future research

Speaking to MNT about the clinical implications of the study, Dr. Swanson said, “Our findings show that it is […] possible to get the anti-inflammatory effect of a ketogenic diet without actually being ketogenic.”

[The keto] diet is difficult to follow […], especially for people who are acutely ill. Our work identifies a potential drug target that can produce the same effect as [the] ketogenic diet.”

“I think the work also increases the scientific legitimacy of the ketogenic diet/inflammation link,” he added.

Dr. Swanson went on to highlight how important it is that the research conducted by he and his team uncovered a causal mechanism rather than simply pointing to an association.

“Most scientists,” he told us, “are reluctant to accept cause-effect relationships between events in the absence of a defined mechanism. Here we have provided a biochemical mechanism by which diet affect inflammatory responses.”

Dr. Swanson also shared with us some directions for future research. “Our work was very focused on brain trauma,” he said, but “next steps will be to expand the list of pro-inflammatory conditions that can be modulated by the CtBP mechanism.”

The findings could apply to other conditions that are characterized by inflammation. In diabetes, for example, the excessive glucose produces an inflammatory response, and the new results could be used to control this dynamic.

“[The] ultimate therapeutic goal would be to generate a [drug] that can act on CtBP to mimic the anti-inflammatory effect of [the] ketogenic diet,” Dr. Swanson concluded.

“It’s a key issue in the field — how to suppress inflammation in brain after injury,” said Raymond Swanson, MD, a professor of neurology at UC San Francisco, chief of the neurology service at the San Francisco Veterans Affairs Medical Center, and senior author of the new study.

In the paper, published online September 22, 2017 in the journal Nature Communications, Swanson and his colleagues found the previously undiscovered mechanism by which a low carbohydrate diet reduces inflammation in the brain. Importantly, the team identified a pivotal protein that links the diet to inflammatory genes, which, if blocked, could mirror the anti-inflammatory effects of ketogenic diets.

“The ketogenic diet is very difficult to follow in everyday life, and particularly when the patient is very sick,” Swanson said. “The idea that we can achieve some of the benefits of a ketogenic diet by this approach is the really exciting thing here.”

Low-Carb Benefits

The high-fat, low-carbohydrate regimen of ketogenic diets changes the way the body uses energy. In response to the shortage of carb-derived sugars such as glucose, the body begins breaking down fat into ketones and ketoacids, which it can use as alternative fuels.

In rodents, ketogenic diets — and caloric restriction, in general — are known to reduce inflammation, improve outcomes after brain injury, and even extend lifespan. These benefits are less well-established in humans, however, in part because of the difficulty in maintaining a ketogenic state.

In addition, despite evidence that ketogenic diets can modulate the inflammatory response in rodents, it has been difficult to tease out the precise molecular nuts and bolts by which these diets influence the immune system.

Intricate Molecular Waltz

In the new study, the researchers used a small molecule called 2-deoxyglucose, or 2DG, to block glucose metabolism and produce a ketogenic state in rats and controlled laboratory cell lines. The team found that 2DG could bring inflammation levels down to almost control levels.

This image shows hippocampal slices.

Immunostaining for Iba1 and iNOS identify activated microglia in mouse hippocampal slice cultures after 24 h incubation with LPS (10 μg/ml) or LPS + 2DG (1 mM) NeuroscienceNews.com image is credited to Swanson et al./Nature Communications.

“I was most surprised by the magnitude of this effect, because I thought ketogenic diets might help just a little bit,” Swanson said. “But when we got these big effects with 2DG, I thought wow, there’s really something here.”

The team further found that reduced glucose metabolism lowered a key barometer of energy metabolism — the NADH/NAD+ ratio — which in turn activated a protein called CtBP that acts to suppress activity of inflammatory genes.

In a clever experiment, the researchers designed a drug-like peptide molecule that blocks the ability of CtBP to enter its inactive state —essentially forcing the protein to constantly block inflammatory gene activity and mimicking the effect of a ketogenic state.

Peptides, which are small proteins, don’t work well themselves as drugs because they are unstable, expensive, and people make antibodies against them. But other molecules that act the same way as the peptide could provide ketogenic benefits without requiring extreme dietary changes, Swanson said.

The study has applications beyond brain-related inflammation. The presence of excess glucose in people with diabetes, for example, is associated with a pro-inflammatory state that often leads to atherosclerosis, the buildup of fatty plaques that can block key arteries. The new study could provide a way of interfering with the relationship between the extra glucose in patients with diabetes and this inflammatory response.



How the war on Cholesterol caused our diabetes epidemic


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.


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.


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.


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]


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.


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]


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.


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.


[1] https://themedicalbiochemistrypage.org/cholesterol.php

[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

[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.

[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.

[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.

[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

[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.
Lancet Diabetes Endocrinol 2017 Published Online August 29, 2017 http://dx.doi.org/10.1016/S2213-8587(17)30283-8
PURE lipids and BP

Saturated Fat advice from AHA is still 20 years behind science

The new American Heart Association (AHA) position statement on saturated fat and cardiovascular disease is slightly lesswrong and misleading as previous statements they made. [1]

AHA Presidential

First, we do find some common ground

  1. It seems reasonable to us that specific saturated fats, most notably palmitic acid, can have adverse cardiometabolic effects when combined with refined carbohydrates and eaten by people with an excessive postprandial insulin response.
  2. It also seems reasonable that the effects can be quite different outside of this context, and in fact the AHA has cited evidence that shows this, which we will get to later.

We’re not poo-pooing the whole idea or the body of evidence on display here, just pointing out that the AHA’s single-minded obsession with the 10-15% of saturated fat in the average diet has completely blinded them to the effect of the 50-60% of mostly refined carbohydrate, and the value of replacing that with almost anything. We think that in this case the naturally occurring saturated fat in the diet will be harmless and quite possibly somewhat beneficial at a population level.

So how do you wade through and make any sense of the research evidence the AHA has presented? Here’s our attempt.

Meta-analysis of RCTs (we like)

We can start with the new meta-analysis of saturated fat substitution RCTs that the AHA team has done. We’ve never seen a meta-analysis like this. There seems to be no prearranged protocol. What we get instead is the four most favourable studies of PUFA replacing saturated fat, now designated “core studies” and analysed separately from all the RCTs that failed to confirm the hypothesis, using the fixed-effects model. The unfavourable RCTs are dismissed because of confounders that favoured the control diets. However, confounders that favoured the interventions go unmentioned. Controls in the Sydney Diet Heart study may in fact have consumed more trans fats [TFA] than the intervention group for example, which is consistent with the intervention lowering LDL cholesterol; the AHA hypothesis is that lowering LDL cholesterol reduces heart attacks and heart attack deaths, but this is the opposite of what happened in Sydney.[2]

The AHA has rehabilitated the Finnish Mental Hospital Study and included it as a “core study”, and this tells you a lot about their attitude to the scientific method, which Gary Taubes demolishes here. In the FMHS the populations in two hospitals were allocated to different diets, and the patients who ate a high intake of PUFA (from rapeseed oil) replacing SFA saw fewer heart attacks and cardiovascular deaths. This is the SFA-replacement study with the largest reduction in CHD and CVD mortality in the intervention arm (0.59), which may be why the AHA choose to revive it. However, non-CVD deaths rose and the all-cause mortality rate didn’t go down (1.01).
In any case, it’s our view that this study has  important confounders that the AHA hasn’t mentioned. For example, the patients were treated with a cardiotoxic medicine, thioridazine, with overall greater use in the control diet groups (0.63 vs. 0.97 standard doses/day).[2] Thioridazine is an antipsychotic  drug that causes heart attacks as a side effect, which is why it was withdrawn worldwide in 2005. The control diet groups were also fed more trans fats than the intervention groups (2%E vs 0%E in hospital K, 0.6%E vs 0.2%E in hospital N).[2] So the people eating more PUFA may have had fewer heart attacks because of the PUFA, which is plausible because this diet supplied plenty of omega 3 to a population possibly lacking in it, but for all we know it could have been due to the fact that they were being poisoned less often. Or, of course, just due to chance, because this study wasn’t fully randomised a a patient level. Patients were allocated diets on admission to hospital and there were only two hospitals; this is called a cluster trial and it takes more clusters than were in FMHS to equate to a randomised trial.

Now, either the AHA knows about the confounding, and they should, it’s been mentioned in discussions of this trial for years (including their ref. 35) and Steven Hamley covers it in his own recent meta-analysis – the one that tried hardest to account for confounders, and they’ve chosen not to mention it. The alternative is that they don’t know, and are sleepwalking through the science with blinkers on. In general – and probably in toto – the AHA meta-analysis covers only half the evidence on confounders, the half that suits the AHA position, as Gary Taubes found when he analysed the Oslo study. We ask how this gets past independent peer-review?

Fat intolerance and its causes

We don’t have time to check every reference, but as usual we checked the ones that claimed to prove something of interest to us. One of these is the primate studies in which saturated (and monounsaturated) fat is more atherogenic than PUFA (studies in mice and rabbits don’t show this consistently enough to validate the hypothesis). The AHA states:

“To induce hypercholesterolemia and atherosclerotic lesion formation, one group of monkeys typically was fed lard or palm oil at 35% of their daily energy intake and dietary cholesterol to raise serum cholesterol levels into the 300- to 400-mg/dL range to model hypercholesterolemia in human beings at high risk for CHD. A second group of monkeys was fed a monounsaturated fat, high-oleic safflower oil, and a third group was fed a polyunsaturated fat linoleic acid–rich diet using safflower oil. Saturated fatty acids promoted higher LDL cholesterol concentrations and more coronary artery atherosclerosis. Linoleic acid lowered LDL cholesterol concentrations and decreased the amount of coronary artery atherosclerosis.”

How much cholesterol do you need to feed to monkeys to make them intolerant of saturated (and monounsaturated) fat? 0.8mg/Kcal; the equivalent of 1,600mg for a human eating 2,000kcal/day.[3] This is more cholesterol than you should make in an average day, so the monkey cannot downregulate cholesterol synthesis enough to compensate. Humans, with natural diets higher in cholesterol, can usually decrease absorption of cholesterol and increase excretion enough to tolerate such amounts. Indeed in some cases much larger amounts –  but these monkeys can’t.[4] However, the test monkeys were chosen for their response to saturated fat and cholesterol in the first place, they weren’t chosen at random from the monkey population. Monkeys that didn’t respond as desired were excluded from the study.[3] It’s not the saturated fat causing atherosclerosis, or these monkeys would only have needed to be fed saturated fat.

Here’s a question; what factor, if any, could possibly make a human as intolerant of fat as a cholesterol-fed monkey? Surely not fat itself, nor the minor amounts of cholesterol in the average human diet. How about the insulin response to refined carbohydrate? High refined carb diets cause heart disease in monkeys without any need to feed them cholesterol. This is the elephant in the room with the AHA. They do mention that replacing SFA with refined carbs is a bad idea (despite the AHA having recommended this substitution for many decades). You get the impression that they only think it’s bad because it has no effect, not because it’s harmful – more on this later.

Another cause of high cholesterol

In a 1991 cross-over trial, 147 non-obese normotensive subjects (60 females and 87 males) aged 19-78 were placed alternately on high-sodium and low sodium diets. The high sodium diet raised mean arterial blood pressure by a mean of 7.5 mmHg in 17% of the subjects (salt sensitive) – the low sodium diet raised mean arterial blood pressure by a mean of 6 mmHg in 16% (reverse reactors). With dietary salt restriction serum total- and LDL-cholesterol as well as serum insulin and uric acid concentrations increased significantly in all three groups. The largest increases in total (10%) and LDL- (12%) cholesterol occurred in the reverse reactors.[5]

So it would appear that the salt restriction advice the AHA has been giving generally for years, in the face of growing contradictory evidence, can raise cholesterol as much as eating butter can if taken to extremes. Again this is ignored.

Evidence that SFA is safe in low carb diets is cited but concealed

As an example of the AHA”s approach to evidence, consider the reference for this claim.

“Therefore, the effects of replacing carbohydrates with various kinds of fats qualitatively at least may be similar by increasing larger and decreasing smaller LDL sizes. In another study, monounsaturated fat, replacing carbohydrates, reduced medium and small LDL, also shifting the distribution to the larger size.78”

In the context in which it occurs, the statement is far from exciting, but the reference 78 is actually a very valuable experiment and one of the few that answers the question “what is the difference between high saturated fat and low saturated fat in a low carb diet?” This should be something that interests the AHA, but the blinkers mean they can only use this paper to buttress their own position on some minor point while ignoring the main outcomes from this research.

Ref 78 is a Ron Krauss paper in which a low fat diet (54% CHO) is compared with a moderate fat diet (39% CHO) and two low carb (26% CHO) diets, one with 15% SFA, one with 9% SFA. The diets are isocaloric, and the 15% SFA diet is superior to all other diets for four cardiometabolic results. Lower triglycerides, higher HDL, lower total cholesterol/HDL ratio, lower ApoB/ApoA1 ratio, larger LDL particle size.[6,7]

total C HDL

Now, the AHA is quite churlish about particle size. Maybe they’re right, maybe they’re wrong. However, every LDL particle only has one ApoB lipoprotein. The larger the particles, the less ApoB you have at any given LDL concentration. The ApoB/ApoA1 ratio (only slightly) favours the 15% SFA diet. Of course, 26% CHO is a little outside the upper edge of low carb, but this is the best evidence we have to show whether SFA in a low carb diet is a worry or not. The evidence says it’s not. In fact, what this study shows is that carbs are are mechanistic in causing poor lipid profiles as related to cardiometabolic health.

The evidence on carbohydrate

The AHA review also cites observational studies, including the Jakobsen et al and Farvid et al meta-analyses, in which a substitution analysis appears to show that replacing saturated fat with mostly linoleic acid is beneficial. The logic of this is impeccable – “because we can’t find the evidence that we wish existed, that saturated fat is independently associated with heart disease (which would suggest a causal relationship), we are going to compare it with the essential fatty acids, because that makes it look worse”. These studies are out of date because they do not include the two Praagman et al studies from last year, in the larger of which (n=35,597) replacing SFA with PUFA was associated with an increase in ischemic heart disease events.[8]

“Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27-1.37).”

In the smaller (n=4,722) study there was no association.[9]

Even so, what do the substitution meta-analyses tell us? That every benefit, if there is a benefit, of replacing SFA with PUFA can also be achieved by replacing carbohydrate with PUFA. By carbohydrate is meant the total carbohydrate from the mixture of refined (flour, sugar) and unrefined (potato, fruit, whole grains, legumes) sources in the usual diet. The AHA fastens on this distinction – not made in the substitution metas – to tell us that replacing 5% of energy from saturated fat with 5% of energy from whole grains will produce some huge associational benefit.

If your diet was about 50% refined carbohydrate, as is normal in Western countries these days, you’d be looking to replace some of that with unrefined carbs, PUFA, MUFA, anything at all, rather than worrying about the 10-15% of saturated fat left in these diets!
Let’s look at this again – you have maybe 50% of energy from junk carbs to replace in the Standard Western Diet. You don’t need any of it – you can replace every last bit of it and only feel better for the effort.

On the other hand you have around 15% of saturated fat at most. Much of this is attached to whole foods – some of it is even in nuts, fish, and vegetable oils!
Priorities, people, priorities.

Even Harvard’s NHS/HPFS study, which has its issues but which the AHA relies on heavily here, predicts that replacing carbs (which includes some unrefined) with fat (which includes some saturated) will be associated with lower mortality, 0.84 (0.81-0.88) and cardiovascular mortality, 0.86 (0.79, 0.93).[10] Similarly, the Malmo Diet and Cancer Study found a significantly lower risk of CVD death (RR 0.65, p=0.028) in men eating the most fat, an average of 47%E.  “No deteriorating effects of high saturated fat intake were observed for either sex for any cause of death”.[11]

But supposing there is a benefit of PUFA? The Farvid meta-analysis predicted that “A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events (RR, 0.91; 95% CI, 0.86-0.96) and a 13% lower risk of CHD deaths (RR, 0.87; 95% CI, 0.82-0.94).”[12] One good wholefood source of linoleic acid is nuts. According to a 2016 meta-analysis, just eating 28g of nuts per day was associated with greater decreases in mortality from coronary heart disease, 0.71 (95% CI: 0.63–0.80), cardiovascular disease, 0.79 (95% CI: 0.70–0.88), and all-cause mortality, 0.78 (95% CI: 0.72–0.84) than those predicted by Farvid et al for total PUFA.[13] We have this evidence that PUFA from nuts is beneficial, or at least not harmful. We don’t actually have the same evidence when it comes to PUFA from plant seed oils – no-one has looked at these specifically.

Coconut oil – the rush to judgement

When Ancel Keys chose his 7 countries to study from the 22 or 23 available, he chose Japan as an example of a country with a low fat intake and a low rate of heart disease; but he could have chosen Ceylon, very close to it on the graph, with a similar low rate of heart disease but 4x as much saturated fat as Japan, because the Ceylonese cooked with coconut oil.

As an aside, a recent cohort of 58,472 Japanese followed up 19 years with 11,656 deaths showed that Japanese women with the highest saturated fat intake, and higher total fat intake had lower mortality rates. So, for what is worth, there is some associational evidence that more fat could be protective in the Japanese population.[14]

We don’t know a lot more about coconut oil today than we did in Ancel Key’s day, but the AHA thinks that its effect on serum lipids warrants avoiding it. That makes sense in a country where having higher cholesterol increases the risk of being prescribed unnecessary drugs or having your insurance premiums raised. Viewed in that context, coconut oil could be truly hazardous to your health.

Most of the health claims made for coconut oil can’t be substantiated, because the research hasn’t been done. An exception is this recent paper, which shows that a meal high in coconut oil had a more favourable effect on postprandial lipids than either palm oil or rice bran oil.[15] It’s also interesting because it shows that higher insulin and a higher fasting TG/HDL ratio (1.8 vs 1.1) is associated with an adverse response to palm oil. We’d interpret this as meaning that carbohydrate intolerance (the meal supplied an OGTT dose of refined carbs) drives fat intolerance, as we would expect from the interaction between carbohydrate, insulin, and palmitic acid discussed here.
Another benefit of using coconut oil for meals such as stir fries is that it is much less likely than plant seed oils to produce carcinogenic fumes. Lung cancer risk is greatly increased in non-smokers exposed to heated seed oils in poorly ventilated kitchens, as we discussed here.

The Dog in the Manger

One of the defects of the modern “Presidential” personality type, as we mentioned in the introduction, is that every innocuous question is treated with a partisan bias. Nowhere is this more evident than in the handling of trans fats.

Industrial trans fats probably increase heart disease risk, more by their effect on the metabolism of omega-3 and -6 fatty acids and how this affects blood clotting and inflammation than by any effect on lipids or basic metabolism.

Fact – people were only exposed to industrial trans fats because animal fats were replaced with vegetable fats.

There are also trans fats in dairy – ruminant trans fats. These, as far as we can tell, are associated with better health not worse

The AHA really wants (you) to believe that the effects of ruminant trans fats are similar to those of industrial trans fats.

“Although most human trials were conducted with partially hydrogenated vegetable oil, emerging evidence suggest the ruminant trans fatty acids have similar adverse effects on blood lipids…Although industrial trans fatty acids were consistently associated with total CHD and CHD death in observational studies, ruminant trans fatty acids were generally not. The exact reason for these discrepant relationships remains unknown but may relate to the very low levels of ruminant trans fatty acids in these studied populations (mean intake, ≈0.7% of total energy),112 differences in trans fatty acid isomers between ruminant and industrial trans fatty acids that have diverse biological effects, or confounding by the high amount of saturated fat in the major source of ruminant trans fatty acids.”

Firstly, ruminant trans fats (present in both dripping and dairy fat at around 3%) are products of the fermentation of plants by bacteria. Does anyone still believe that such fermentation is bad for the heart? The dominant ruminant trans fat, CLA, is a cis-trans fat. The cis bond means that it cannot behave like an industrial trans fat in cell membranes. The metabolism of CLA in vivo involves elongation and further desaturation similar to that seen with long-chain polyunsaturates.

The “emerging evidence” that the AHA alludes to involves feeding doses of ruminant trans fats higher than those sourced from diet in supplement form, without their accompanying fats. This is a critical point; the myristic acid in ruminant fats raises the most beneficial forms of HDL, but the benefit of HDL depends on its functionality. Ruminant trans fats by themselves increase HDL functionality, but not mature HDL.[16] The similar benefit of olive oil and red wine polyphenols may also depend on their inclusion in foods that raise HDL.[17]
Whole foods beat supplements and refined foods every time.

Interventions in Children

The AHA review mentions a number of intensive healthy-lifestyle interventions in children that reduced saturated fat, always in the context of many other changes including reduced sugar, and had positive effects on various proxies for heart disease risk. We concur that healthy diet and lifestyle choices can overall reduce heart disease risk. What we don’t know is whether saturated fat intake from good-quality sources needs to be restricted to produce these benefits, and whether greater benefits will not in fact follow from a higher fat, lower refined carbohydrate diet that minimises insulin exposure after meals. The least-confounded RCTs of saturated fat reduction suggest that it contributes little if any benefit in adults, and the evidence that specifically relates to low fat vs whole milk, and to fat content overall in the diet of children (including breast-feeding infants, which eliminates reverse causality), suggests that lower fat foods and diets in the general population are associated with higher childhood BMI and therefore greater future cardiovascular risk.[18-23]

Summing up

The recommendation to eat less than 30% of energy as fat, applied to a population with easy access to refined carbohydrates, as promoted by the AHA (which did promote the use of sugar and flour in place of naturally fatty foods for many years) may have increased fat intolerance in the population, mostly with regard to specific saturated fats, mainly palmitic acid.[24] This intolerance, because it is driven by insulin, seems to go away when carbohydrate is restricted. It may also go away to some extent when genuinely unrefined carbohydrate replaces refined starch and sugar, due to the lower insulin AUC.

It would literally take a PhD thesis to fully dissect the AHA presidential advisory and its errors of interpretation and expressions of bias. We’ve only dipped into the areas we already know about, and found the AHA trying to pull a fast one. Which is not to say that every statement or idea in the document is false, but that half the story is hidden in darkness. The public needs bodies like the AHA to adjudicate fairly, not act like a prosecutor for one cause then a defense attorney for another. The AHA’s diet advice may be taken with a grain of salt by many in the know who can afford to ignore it, but not by those fed in institutions or by government programs, and the AHA’s stated positions also influence drug prescribing. If the AHA can’t balance the evidence wisely, and step well beyond the bias of defending their previous assumptions that a high carb, low fat diet low in saturated fat is best for all, we’re in trouble.



[1] Sacks FM, Lichtenstein AH, Wu JHY et al. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. 

[2] Hamley S. The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutrition Journal. 2017; 16:30 DOI: 10.1186/s12937-017-0254-5

[3] Rudel LL, Parks JS, Sawyer JK. Compared with dietary monounsaturated and saturated fat, polyunsaturated fat protects African green monkeys from coronary artery atherosclerosis. Arterioscler Thromb Vasc Biol. 1995;15:2101–2110.

[4] Kern F. Normal Plasma Cholesterol in an 88-Year-Old Man Who Eats 25 Eggs a Day — Mechanisms of Adaptation. N Engl J Med. 1991; 324:896-899. DOI: 10.1056/NEJM199103283241306

[5] Ruppert M, Diehl J, Kolloch R et al. Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Klin Wochenschr. 1991;69 Suppl 25:51-7.

[6] Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT.
Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia [published correction appears in Am J Clin Nutr. 2006;84:668]. Am J Clin Nutr. 2006;83:1025–1031; quiz 1205.

[7] Feinman RD, Volek JS. Low carbohydrate diets improve atherogenic dyslipidemia even in the absence of weight loss. Nutrition & Metabolism. 2006; 3:24 DOI: 10.1186/1743-7075-3-24

[8] Praagman J, Beulens JW, Alssema M et al. The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition-Netherlands cohort.Am J Clin Nutr. 2016; 103(2): 356-365.

[9]Praagman J, de Jonge EAL, Kiefte-de Jong JC et al. Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population.

[10] Wang DD, Li Y, Chiuve SE, Stampfer MJ, Manson JE, Rimm EB, Willett WC, Hu FB. Association of Specific Dietary Fats With Total and Cause-Specific Mortality. JAMA Intern Med. 2016;176(8):1134-1145. doi:10.1001/jamainternmed.2016.2417.

[11] Leosdottir M, Nilsson PM, Nilsson JA, Månsson H, Berglund G. Dietary fat intake and early mortality patterns–data from The Malmö Diet and Cancer Study. J Intern Med. 2005 Aug;258(2):153-65.

[12 Farvid MS, Ding M, Pan A et al. Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. 

[13] Aune D, Keum N, Giovannucci E et al. Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies. BMC Medicine. 2016; 14:207
DOI: 10.1186/s12916-016-0730-3

[14] Wakai K, Naito M, Date C, Iso H, Tamakoshi A. Dietary intakes of fat and total mortality among Japanese populations with a low fat intake: the Japan Collaborative Cohort (JACC) Study. Nutrition & Metabolism. 2014;11:12. doi:10.1186/1743-7075-11-12.

[15] Irawati D, Mamo JCL, Slivkoff-Clark KM et al. Dietary fat and physiological determinants of plasma chylomicron remnant homoeostasis in normolipidaemic subjects: insight into atherogenic risk. British Journal of Nutrition (2017), 117, 403–412. doi:10.1017/S0007114517000150

[16] Nicod N, Parker RS, Giordano E et al. Isomer-specific effects of conjugated linoleic acid on HDL functionality associated with reverse cholesterol transport. J Nutr Biochem. 2015 Feb;26(2):165-72. doi: 10.1016/j.jnutbio.2014.10.002. Epub 2014 Nov 12.

[17] Nicod N et al. Green tea, cocoa, and red wine polyphenols moderately modulate intestinal inflammation and do not increase high-density lipoprotein (HDL) production. J Agric Food Chem. 2014; 62(10):2228-32. doi: 10.1021/jf500348u. Epub 2014 Mar 4.

[18] Prentice P, Ong KK, Schoemaker MH, et al. Breast milk nutrient content and infancy growth. Acta Paediatrica (Oslo, Norway : 1992). 2016;105(6):641-647. doi:10.1111/apa.13362.

[19] Vanderhout SM, Birken CS, Parkin PC, Lebovic G, Chen Y, O’Connor DL, Maguire JL; TARGet Kids! Collaboration. Relation between milkfat percentage, vitamin D, and BMI z score in early childhood. Am J Clin Nutr 2016;104:1657–64.

[20] Rolland-Cachera MF, Maillot M, Deheeger M, Souberbielle JC, Peneau S, Hercberg S. Association of nutrition in early life with body fat and serum leptin at adult age. Int J Obes (Lond) 2013;37:1116–22.

[21] Alexy U, Sichert-Hellert W, Kersting M, Schultze-Pawlitschko V. Pattern of long-term fat intake and BMI during childhood and adolescence—results of the DONALD study. Int J Obesity Relat Metab Dis. 2004;28: 1203–9.

[22] Gunnell DJ, Frankel SJ, Nanchahal K, et al. 1998. Childhood obesity and adult cardiovascular mortality: a 57-year follow-up study based on the Boyd Orr cohort. American Journal of Clinical Nutrition 67: 1111–18.

[23] Ness AR, Maynard M, Frankel S, et al. Diet in childhood and adult cardiovascular and all cause mortality: the Boyd Orr cohort. Heart. 2005;91(7):894-898. doi:10.1136/hrt.2004.043489.

[24] Kuipers RS, de Graaf DJ, Luxwolda MF et al. Saturated fat, carbohydrates and cardiovascular disease. Neth J Med. 2011 Sep;69(9):372-8.

Glucose Ketone Index (GKI) – What Ratio Do I need for Nutritional Ketosis Benefits?

Generally these blog posts are a result of scratching my own itch (answering my own question), and this post is no different.

At the time of writing this, I’m doing a 5-day fast, and wanted to understand the readings I’m getting for my blood glucose and blood ketone levels.

Initially I thought that blood ketones were all that mattered, and certainly a lot of people only talk about that reading. But looking at Dr Thomas Seyfried’s paper on treating brain cancer (glioblastomas).  It suggests that its important to take into account blood glucose also. In their study, they acheieved optimal results when their patients maintained what they called ‘nutritional ketosis’. And as part of the paper, they included a formula for what this means.

The chart below describes visually what they mean by nutritional ketosis, and how it affected the tumour growth. The red is an increase in ketones as a fictional patient goes deeper into ketosis. The black line represents blood glucose, that decreases to a plateau, as carbohydrate sources are removed from the diet, and glycogen stores decrease.

So that sweet spot they reach at the end is an optimum level of nutritional ketosis. Now… obviously in our case we are (hopefully) not trying to slow the growth of a glioblastoma. But by getting into ketosis we’re hoping to achieve a number of benefits including:

  • Reduced IGF-1
  • Immune system rejuvenation (perhaps mainly lymphocytes)
  • Increased cellular autophagy
  • Reduced inflammation (often measured by improved C-reactive protein levels)

The extent of these benefits will depend if you’re eating a keto diet, or doing a water fast/fast mimicking diet. But all 3 should improve the biomarkers such that you have a reduced risk of major diseases such as diabetes, cancer and cardiovascular disease.

And studies like this one indicate that the optimal benefits from ketosis lie in maintaining  a 1:1 or lower ratio of glucose to ketones.

So on to the crux of this post, how to calculate GKI. What you’re trying to do is compare apples with apples, you really really want both readings in mmol/L. In my case, having a meter sourced from the UK, that’s how they came, so I simply do:

Glucose Reading (mmol/L) ÷ Ketone Reading (mmol/L)

However, if you’re in the USA, your blood glucose reading will be in mg/dL. You’ll know, because the meter should say mg/dL. But to be sure, if you blood glucose is in the 100s as a score, rather than single digits, that’s likely mg/dL.

So you’ll want to convert that glucose reading into mmol/L by doing:

Your Glucose Reading (mg/dL) ÷ 18.02

This converts your reading from mg/dL into mmol/L, and then you can do the above calculation (glucose reading divided by ketone reading) to get your glucose ketone index score.

So that’s it really, pretty simple.

Links that may be of use:

1 – Thomas Seyfried et al’s paper on using the glucose ketone index to treat brain cancer:
The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer

2 – An excel calculator for the GKI, developed by Dr Seyfried’s colleague Joshua Meidenbauer:
Glucose Ketone Index Calculator

What sticks out for me with all this stuff, is how amazingly valuable it can be in our treatment (and prevention of cancer), and yet in 2017 an incredibly small number of people (& physicians!) know and understand this work. For those with cancer, if its combined with other treatments, its even better. Its 5 years since Thomas Seyfried published his book ‘Cancer as a Metabolic Disease’. Time will tell how fast we are able to communicate this “meme” to a wider audience.

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.


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.


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.


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


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!

Carbohydrates, Not Saturated Fat, Are Correlated with Cardiovascular Disease

We’ve been told for many decades now to avoid saturated fat to lessen our risk of heart and other cardiovascular disease. But as with so many other pieces of mainstream health wisdom, the doctors and scientists got that one wrong, not that there was such great evidence to begin with. Instead, their recommended macronutrient, carbohydrates, not saturated fat, are correlated with cardiovascular disease. It’s time to end the lies.

What the Health

You may have heard of the new documentary film “What the Health”, which blames meat for the epidemic of obesity, diabetes, and heart disease, and advocates veganism for health.

I can’t review this movie because I saw only some of it. I had to leave the room after watching some of it because I couldn’t stand the incredible mendacity on display in both the interviewees’ answers and the tone of the film. In any case, seeing some of it and realizing how popular it’s become prompted this article. Most people, not knowing any better, take that stuff at face value because of doctors in the film and because it confirms their biases about meat. (Nina Teicholz wrote a solid takedown of the film’s lack of a base in actual science.)

Saturated fat does not cause heart disease

In a recent article, we saw that red meat, contrary to what you’ve heard for years, is a health food.

The main component of meat that’s been thought to be involved in cardiovascular disease is saturated fat.

Yet, a recent meta-analysis (an analysis of other studies) found, “Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes…”

The study did find an association of a particular type of fat with all-cause mortality as well as coronary heart disease, and that was trans fat, the type found in hydrogenated vegetable oils used in processed foods.

Another study from a few years ago, one of whose authors was Ronald Krauss, a very big name in this field, concluded, “… there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

The doctors in “What the Health” must be aware of these studies; if so, they’re being willfully misleading, and if not, are willfully ignorant.

It beggars the imagination that a food that humans have eaten for millions of years, sometimes to the exclusion of anything else, suddenly causes heart disease and obesity. The consumption of red meat has actually declined since before the obesity epidemic (although poultry consumption has increased), and the consumption of grains has increased. See the following chart (source).



Carbohydrate consumption is linked to cardiovascular disease

If saturated fat isn’t linked to the incidence of cardiovascular disease, the biggest killer in the developed world, what is?

Carbohydrates, especially refined carbohydrates from grains.

A study that was published last year, Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries, found that “The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption.”

Yes, you read that right. The more fat and the more animal protein people ate, on a population basis, the less cardiovascular disease they had.

The study also found that “The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates.” [My emphasis.]

The following chart illustrates the correlation between the amount of carbohydrates (and alcohol) in the diet, by country, and the total CVD mortality in women.


The study found that animal fat did indeed raise cholesterol levels, but that “the relationship between raised cholesterol and CVD indicators in the present study is always negative.” The higher the cholesterol, the lower the CVD rates.

The major correlates of high CVD risk were:

  • carbohydrates, especially refined, high-glycemic carbohydrates (potatoes, cereal grains, sugar)
  • distilled liquor
  • sunflower oil

The major correlates of low CVD risk were:

  • fat and protein intake
  • fruits and wine
  • vegetables

As always, correlation does not equal causation. Other important factors relating to CVD deaths that this study found were smoking, BMI, and level of healthcare expenditure.

But these associations appear to exonerate saturated fat from animal sources, such as meat and dairy, from causing heart disease and stroke. And they imply that carbohydrates are a problem.


The above-cited study states, “The obvious fallacy of the ‘saturated fat hypothesis’ can be demonstrated by the example of France – a country with the highest intake of animal fat in the world and the second lowest CVD mortality (after Japan).”

Ergo, saturated fat does not cause cardiovascular disease, despite what the makers of “What the Health” would have you believe. The film is just more lies from the mainstream.

The authors also state,

Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.

Why would carbohydrate consumption be associated with CVD? Likely because they can lead to insulin resistance, which is probably the true cause of heart disease, as well as a major risk factor for cancer.

So eat meat in the knowledge that can improve your health, not decrease it, and cut back on the consumption of refined carbohydrates.

Added 7/24/17: There’s another ongoing study, results apparently not published yet, the PURE study, led by Salim Yusuf, M.D., a prominent cardiologist. The PURE study is also epidemiological like the above cited study, and exonerates saturated fat and points toward carbohydrates as increasing the risk of CVD. Dr. Michael Eades discusses it here.


This article was written and published on roguehealthandfitness.com, and has been reproduced here in its entirety.

Keto Diet fights cancer and heart disease for longer and healthier life


Health Benefits of Ketones

A ketogenic diet is characterized by the production of ketones, small molecules that the body can use as alternative energy sources. These molecules — beta hydroxybutyrate, acetoacetate, and acetone — are produced when carbohydrate consumption is very low. Depletion of glycogen, the storage form of carbohydrate, results in the production of ketones from fatty acids.

Intermittent fasting also causes the production of ketones, since if you’re not eating anything, you’re not eating carbohydrates either.

How low does carbohydrate consumption need to be to cause the production of ketones? The amount varies, and most people will need to eat 50 grams or fewer carbohydrate daily to see a rise in ketones. People who are very physically active, such as through daily strenuous exercise, may be able to eat 100 grams or more and still be in ketosis.

Ketones are used as an alternative to glucose. The body only carries about a 24-hour supply of glycogen — which is broken down to glucose — but the supply of fat is enough to last for weeks or months, depending on how much fat the person has. So after a period of about 24 hours with minimal carbohydrate intake, the production of ketones ramps up.

Just to be clear, the ketones under discussion here have nothing to do with raspberry ketones, which are a current weight-loss fad and appear to be ineffective for that purpose.

Health benefits of ketogenic diets

Ketones and the ketogenic diet have a number of health benefits.

  1. The ketogenic diet has strong anti-seizure properties. Many children and adults with epilepsy, whose condition cannot be treated with drugs, become seizure-free with a ketogenic diet.(1) The effect may be due to increased mitochondrial energy production in the brain.
  2. Ketones and the ketogenic diet may be useful in the treatment of Alzheimer’s disease.(2) A case that was in the news not long ago was of a doctor who treated her husband’s Alzheimer’s disease with coconut oil, which metabolizes to ketones. The treatment was quite successful.(3)
  3. The ketogenic diet may be useful for insulin resistance.(4)
  4. The ketogenic diet may help treat cancer.(5) Cancer cells thrive on glucose, so keeping blood sugar low may be therapeutic.
  5. Finally, the ketogenic diet can be used for fat loss, the Atkins diet being a notable example.(6)

The benefits of the ketogenic diet could be due to several things, for example to the absence of carbohydrate, to the presence of ketones, a decrease in insulin, or even increased consumption of fat. Or possibly to all of these.

The absence of carbohydrate in the diet leads to lower insulin levels, and this in turn allows fat to leave fat cells and be burned as energy. Hence the fat-loss effect of low-carbohydrate diets.

As noted, after 24 hours or more of carbohydrate restriction, ketones begin to be produced, and the presence of ketones and not the absence of carbohydrate seems to be the cause of the beneficial effects of the ketogenic diet in epilepsy and Alzheimer’s.

Ketones suppress hunger

It’s also widely suspected that ketones suppress hunger. They may be the cause of the absence of hunger during prolonged fasting. Many people report that as they begin to fast, they’re hungry, but their hunger goes away as they extend their fast.

The disappearance of hunger has certainly been my experience in fasting, especially if the fast lasts more than about 16 hours. What’s probably happening is that ketone levels increase in the bloodstream, and this suppresses hunger.

The fact that many of the benefits of the ketogenic diet may be due to the ketones themselves opens the way for exogenous ketone supplements. In theory, someone could take one of these supplements to get the benefits without even restricting their carbohydrate intake.

Exogenous ketone supplements

I recently received a sample of KetoCaNa, an exogenous ketone supplement.

KetoSports Keto CaNa


KetoCaNa contains beta hydroxybutyrate, one of the ketones normally produced by a ketogenic diet, and is flavored (“natural flavors”) and sweetened with stevia, a non-caloric sweetener.

I’ve used it several times now, and I can report that it works.

Works for what?

For one thing, it suppresses hunger, just as suspected. I’ve taken it several times in the morning during an intermittent fast. Hunger just goes away.

I’ve also taken it (twice) before lifting weights. Ketones may possibly be used as an alternative fuel during exercise, and thus may boost exercise performance.(7) My own experience here is less definite. Maybe it works. But the high-intensity protocol that I’ve begun practicing lately is so short — typically under 40 minutes — that I probably don’t need an alternative fuel source. I suspect that in a longer exercise bout, say cycling or running, ketones may make more of a difference. But I don’t know, since I don’t do those things.

By suppressing appetite, KetoCaNa could be useful for weight loss. Ketone supplements lead to lower body weight in rats.(8)

One drawback of KetoCaNa: the stuff is expensive. A full serving will run you over $4.00. However, half a serving seems to work well too.

The best way to use it is to take it during a fast, so ketone levels are increased. It will increase ketones if you’ve been eating as well, but that would negate many of the weight-loss benefits.

KetoCaNa may prove to be useful in treating Alzheimer’s, cancer, and epilepsy, but that remains to be seen. Most of those who take it now seem to be athletes.

There’s a newer entry into the ketone supplement line, Pruvit Keto // OS. I haven’t tried it.

MCT oil

Another, cheaper way to raise ketone levels is with MCT oil, which consists of medium-chain triglycerides which rapidly metabolize into ketones. MCTs seem to be difficult or impossible to store as fat, and a diet that included MCT oil resulted in significantly more fat loss than did a diet that contained olive oil, in humans.(9)

A tablespoon of MCT oil ought to do the job. Some people report stomach upset with MCT oil, but it’s never bothered me.

Another good reason to take exogenous ketones or MCT oil during an intermittent fast is because ketones stimulate autophagy, the cellular self-cleansing process.(10)

Increased autophagy is one of the main health benefits of intermittent fasting, and is mainly responsible for its longevity-promoting effect. Adding exogenous ketones while fasting ought to boost the autophagy process even more than fasting alone.


Many of the benefits of a very low carbohydrate ketogenic diet may be due to the presence of ketones. Exogenous ketone supplements can a) provide ketones even when not refraining from carbohydrates, and b) boost ketones even further when eating a ketogenic diet.

Lots of people who suffer from illnesses such as cancer or Alzheimer’s simply will not stop eating carbs. Crazy, I know, because if I had cancer I would do everything I could to treat it. But even a simple measure like cutting carbs seems beyond the reach of many. So ketone supplements may be able to fill in a gap in these cases.

Ketosis extends lifespan


ketosis extends lifespan

Ketosis and ketone bodies

Ketone bodies are the small molecules that are produced by the liver when the body is in a state of ketosis. These can be readily used by the body and, most notably, the nervous system, and one of their functions is to spare lean tissue during ketosis, since with the burning of ketones, the body does not have to break down muscle in order to make blood glucose.

The state of ketosis is readily entered when severely restricting carbohydrates in the diet for just a short while; for instance, if someone goes on the Atkins diet, or generally keeps carbs below 50 grams a day. (If one exercises a lot or is otherwise physically active, one can eat more carbs, say up to 100 grams, and remain in ketosis.)

Ketosis extends lifespan in C. elegans

It turns out that in the roundworm C. elegans, one of the ketone bodies, beta hydroxybutyrate, extends lifespan: D-beta-hydroxybutyrate extends lifespan in C. elegans.

βHB supplementation extended mean lifespan by approximately 20%. … βHB did not extend lifespan in a genetic model of dietary restriction indicating that βHB is likely functioning through a similar mechanism. βHB addition also upregulated ΒHB dehydrogenase activity and increased oxygen consumption in the worms.

So, the ketone functioned similarly to dietary restriction, increased lifespan by 20%, and caused increased metabolism.

It looks like being in ketosis much of the time could be, gasp, good for you.

The probable future Nobel Laureate Cynthia Kenyon discovered that a mutation in insulin signalling in C. elegans caused radically increased lifespan. When she made that discovery, she herself went on a low-carbohydrate diet.

So, add all this to the evidence for the healthiness of a low-carbohydrate diet.




Longer Life Through Lower Blood Sugar

Many experiments and studies on life extension have found the interesting and important result that lowering blood glucose (blood sugar) and/or restricting dietary carbohydrates means longer life. This has been found using several different lab animals and in humans as well. It’s possible to have longer life through lower blood sugar.


Acarbose is an anti-diabetic drug that works by inhibiting enzymes in the gut that break down carbohydrates to glucose, and therefore less glucose is absorbed.

Male mice that were fed acarbose lived 22% longer than controls, although the female mice lived only about 7% longer.


A lifespan increase of 22% is large, among the longer lifespan extensions seen with other interventions, comparable to rapamycin and a larger increase than fat-tissue insulin receptor knockout. Acarbose reduced fasting insulin in male mice but not in females, which may account for the difference in lifespan extension.

IGF-1 was decreased in both sexes, and fibroblast growth factor 21 (FGF21) was increased, and both of these hormonal changes could be involved in life extension.

In humans with type 2 diabetes, long-term acarbose treatment was associated with a huge 50% decrease in the risk of cardiovascular events such as heart attack and stroke. Importantly, the risk reduction was associated with a decrease in postprandial hyperglycemia, or a rise in blood sugar after eating.

A meta-analysis of acarbose found similar large reductions in CVD events.

Since dietary carbohydrates, especially grains, sugar, and starches, are the primary determinant of blood sugar, why not just cut carbohydrates instead?


Metformin is the most prescribed anti-diabetic drug, and it lowers blood sugar and insulin. Similar large reductions in death rates have been found with metformin use, so much so that diabetics using metformin may outlive non-diabetics who don’t use it.

Would cutting carbohydrates cause the same life extension and anti-aging as metformin?

An argument against that is that diabetics taking metformin may live longer than non-diabetics who don’t take it. Therefore, metformin may be causing a real anti-aging effect.

An argument for it is that most non-diabetics eat large amounts of carbohydrates, with the average American eating about 50% of his or her calories as carbohydrate. And among average people, Dr. Joseph Kraft showed that large numbers, perhaps up to 80%, have some degree of impaired glucose tolerance, i.e. they’re insulin resistant.

If metformin increased lifespan in animals or people who ate little or no carbohydrates, that would be convincing, but to my knowledge, it has not.


Glucosamine is an over-the-counter supplement commonly taken for arthritis and joint pain. Glucosamine extends lifespan in mice through

an induction of mitochondrial biogenesis, lowered blood glucose levels, enhanced expression of several murine amino-acid transporters, as well as increased amino-acid catabolism. Taken together, we provide evidence that GlcN [glucosamine] extends life span in evolutionary distinct species by mimicking a low-carbohydrate diet. [My emphasis.]

Glucosamine impairs glycolysis (glucose metabolism) and therefore lowers blood glucose levels.

Glucosamine also activates autophagy, the cellular self-cleansing process that retards aging, and inhibits mTOR, the cellular growth engine that accelerates aging.

In humans, use of glucosamine is associated with an 18% lower death rate.

Again, if glucosamine mimics a low-carbohydrate diet, why not just eliminate the middleman and refrain from eating carbohydrates?


Fasting, eating a very low amount of carbohydrates (usually less than 50 grams daily), or taking ketone supplements or MCT oil raises the amount of molecules known as ketones in the bloodstream. Increased ketones mimic the effects of food restriction by lowering blood glucose and insulin.

While ketone supplements are generally beneficial in my opinion, if you cut the carbohydrates, albeit radically, you’re in ketosis (producing ketones) and presumably extending your lifespan and fighting aging by doing so.


Feeding glucose to the worm C. elegans shortens its lifespan.

Restricting glucose extends its lifespan.

When carbohydrates are digested, they become glucose inside the body, since most carbohydrates are just long chains of glucose. (Sugars may incorporate other molecules, such as fructose and galactose.)

So why not just restrict carbohydrates?

Multiple lines of evidence lead to carbohydrate restriction

As we’ve seen from the studies above, multiple lines of evidence lead to the conclusion that restricting carbohydrates and thus preventing high blood glucose, whether spikes in it or a higher average glucose, leads to longer life.

These same lines of evidence lead to the conclusion that carbohydrates can promote aging and shorten life.

Note that some carbohydrates, namely complex carbohydrates found in non-starchy vegetables, don’t raise blood sugar much if at all.

The foods that contain abundant carbohydrates and increase blood glucose are the ones to restrict or eliminate, and they include grains (wheat, rice, corn, etc.), sugar, and starchy tubers such as potatoes.

Someone who is very insulin sensitive may not be harmed much by carbohydrates. These people include athletes and other lean people who exercise or labor at physically demanding jobs.

Anyone else, and that includes most people, would likely see a big improvement in health by restricting carbohydrates.

Keto Diet Stops Cancer


Cancer is the second leading cause of death in the U.S., and is one of the most dreaded diseases anywhere. It typically strikes older people more; some 90% of cancer is diagnosed in people over the age of 50, and incidence increases with age. Could we be looking at the end of cancer?

While many of the causes of cancer have been identified, the exact manner in which cancer starts and why it does so remains an open question in science. While the lay person may consider the origin of cancer to be of academic interest only, the way that cancer starts, and even precisely what cancer is, has great relevance to prevention and treatment. A new line of thought on cancer has emerged in recent years, backed by compelling evidence, that the prevalent theory of how cancer starts and what it is are wrong, at least in part.

This new way of looking at the problem is the metabolic theory of cancer.

Is cancer caused by genetic mutations?

The prevailing theory of cancer is that it’s caused by genetic mutations, which lead to uncontrolled growth, metastasis, and death. The Mayo Clinic flatly states, “Cancer is caused by changes (mutations) to the DNA within cells.” A scholarly review, The Hallmarks of Cancer, argues that the “enabling characteristic” for these hallmarks of cancer is “genome instability”, that is, the increased propensity of the cell’s genes to mutate.

But seemingly, there’s a paradoxically low rate of mutations together with a high rate of cancer. Even the authors of the review cited above state:

But mutation of specific genes is an inefficient process, reflecting the unceasing, fastidious maintenance of genomic integrity by a complex array of DNA monitoring and repair enzymes. These genome maintenance teams strive to ensure that DNA sequence information remains pristine… Yet cancers do appear at substantial frequency in the human population, causing some to argue that the genomes of tumor cells must acquire increased mutability in order for the process of tumor progression to reach completion in several decades time.

Mutations are rare, they say, because cells strive to repair their DNA, but cancer occurs frequently.

There are a number of other paradoxes of cancer.

The discovery that cancer cells collectively manifest millions of different types of gene mutationsled to the idea that all cancers were different, or different in type, and required complex treatment.

But what if cancer cells all had a remarkable similarity, one that had nothing to do with genetic mutations?

The Warburg effect

Otto Warburg, who won the Nobel Prize for Physiology or Medicine in 1931, first proposed that cancer is due to a metabolic defect.

Just as there are many remote causes of plague, heat, insects, rats, but only one common cause, the plague bacillus, there are a great many remote causes of cancer-tar, rays, arsenic, pressure, urethane- but there is only one common cause into which all other causes of cancer merge, the irreversible injuring of respiration.

In most normal cells, energy is burned in the mitochondria in the presence of oxygen to produce ATP, the currency of energy. Cancer cells have a severely diminished, or no, capacity to do this. Instead, they burn glucose for energy in a process known as aerobic glycolysis. The mitochondria of cancer cells appear to be severely damaged, so the only way they can obtain energy is through this alternative and relatively inefficient method.

Cancer cells burn glucose, as opposed to the mixture of fat and glucose burned by normal cells. Furthermore, non-cancerous normal cells can use ketone bodies for energy, and most cancer cells cannot.

Cancer as a metabolic disease

If genetic mutations don’t cause cancer, what does?

Thomas Seyfried, the most well-known scientist in this area, postulates that cancer is a metabolic disease.

In Seyfried’s view, metabolic dysfunction in the mitochondria of cancer cells is the initial event in cancer formation. The result is genomic instability, leading to the gene mutations seen in cancer; but the mutations are not causal, the metabolic dysfunction is.

Cancer cells burn sugar as a result of their dysfunction.

Therefore, treatment partially consists of depriving cancer cells of glucose. One way to do that is to lower blood glucose levels by the ketogenic diet. In fact, Seyfried has advocated just this approach. It appears to be effective, though much more clinical research would need to be done.

2-deoxyglucose, a compound that is taken up by cells but which cannot be metabolized, and which essentially jams up the metabolic machinery, inhibits cancer cells in vitro. So it appears that depriving cancer cells of glucose, their main fuel, inhibits their growth and may kill them.

Is there any other way to jam the molecular machinery of cancer cells?

Inhibiting cancer metabolism

Enter Dr. Laurent Schwartz, French physician and oncologist, who has been working on this problem for many years and treats patients using the metabolic theory of cancer. (In addition to conventional treatment.)

Schwartz and colleagues have developed a compound called Metabloc, which consists of two over-the-counter (in the U.S. at least) supplements, hydroxycitrate and alpha lipoic acid. These two compounds interfere with the metabolism of cancer cells, but have little effect on the metabolism of normal cells.  Below is a chart showing various strengths of both compounds either alone or in combination against cancer cells in vitro. The highest concentrations of the combination, though still in the micromolar range, reduced cancer cell viability to zero, i.e. no surviving cells.

This treatment, in contrast to standard cancer treatment, is non-toxic, with few side effects.

In vivo, in mice, the combination works too, greatly inhibiting tumor growth. Interestingly, adding another common compound, capsaicin, the substance that gives hot chili peppers their heat, inhibited cancer cells even more. The addition of a fourth compound, a peptide drug called octreotide, further diminished cancer cell viability. Octreotide is a potent inhibitor of growth hormone.

Schwartz has published several papers on the effects in actual patients; the most recent (as far as I know) is “Combination of Metabolic Treatment of Aggressive Primary Brain Tumour and Multiple Metastases of the Brain”.

Background: The combination of hydroxycitrate and lipoic acid has been demonstrated by several laboratories to be effective in reducing murine cancer growth. In previous article in 2014, we reported the fate of 11 patients treated for metastatic cancer unresponsive to chemotherapy. As of today, 32 months after inclusion, five of these patients (45%) are still alive.

Patients and Methods: We report the cases of 12 patients with advanced brain tumor. They were all treated with conventional treatment and a combination of sodium R lipoate (800 mg bid), hydroxycitrate at 500 mg tid and low-dose naltrexone at 5 mg at bedtime. Eight patients had primary brain tumour (n=8 including five glioblastomas) four patients had multiple brain metastases.

Results and Discussion: The combination of conventional and metabolic treatment was well tolerated. Four out of five patients with gliobastoma are still alive and well. The longest follow-up is 7 years.The four patients with disease widely metastatic to the brain have experienced long-term survival. A randomized clinical trial of metabolic treatment associated with conventional treatment is warranted.

The conclusion of the paper states:

To our knowledge, this is the first attempt to treat cancer using a combination of molecules targeting abnormal cancer metabolism. None of these patients experienced major side effects of metabolic treatment. At this stage of development, not a single case proves the efficacy of treatment. But at the time of writing, most patients were alive and well several months after having been sent home to await their death. Several months of life without symptoms strongly suggests that targeting cancer metabolism may be a reasonable option in therapy of advanced brain cancer. The role of metabolic treatment and its association with existing therapy remains to be explored in well-conducted trials.

The end of cancer?

It’s obviously too soon to say whether this new treatment for cancer will be so much of a success that the treatment becomes widely accepted and used. Apparently, Dr. Schwartz is the only oncologist in the world who is using it. His new book is “Cancer: Un Traitement Simple et Non Toxique.”

The number of cancers is increasing and, despite what we hear about medical progress, mortality has not dropped since 1960 , especially for tumors of the pancreas, lungs, liver, brain …

And if, instead of merely seeking to destroy cancer cells with aggressive treatments, they were also rendered functional again? This approach can improve the effectiveness of chemotherapy and the survival of patients.

This is the conviction of Dr. Laurent Schwartz, shared by many scientists around the world. This brilliant physician and researcher in cancer has spent his career gathering evidence that the mechanisms that cause cells to multiply in an anarchic way are essentially related to a sugar burning problem .

In this book written for patients and caregivers, he proposes to normalize the metabolism of cancer cells by a combination of non-toxic and inexpensive foods and supplements, or even a diet low in carbohydrates.

This metabolic treatment has already benefited many patients.

I can only say that if I had cancer, I would definitely seek out the expertise of Laurent Schwartz. He appears to be little known in the U.S., but his latest book will be translated into English and published here. It’s also being translated into Spanish and Italian.


Dr. Laurent Schwartz

While Dr. Schwartz has patented Metabloc, the fact that it’s comprised of two OTC supplements means it’s cheap and that huge pharmaceutical industry profits can’t be made on this treatment. That’s an obstacle to it becoming more widely adopted, since cancer treatment is big business

More Muscle Gains and Fat Loss on a Ketogenic Diet

What happens when you combine weight lifting with a very low carbohydrate ketogenic diet(VLCKD)? You get greater muscle gains and more fat loss than when compared to a conventional diet.

The study looked at a group of “college aged resistance trained men”, and put them on either a conventional Western diet or a VLCKD.

The conventional diet was 55% carbohydrate, 25% fat, and 20% protein, similar to what lots of people eat, though a bit higher in protein, a bit lower in fat.

The low-carb diet was 5% carbohydrate, 75% fat, and 20% protein.

Note that protein, the main macronutrient responsible for muscle growth, was the same in both groups. Both groups did resistance training three times a week for 11 weeks.

The very low carbohydrate group gained twice as much muscle as the conventional group, 4.3 kg vs 2.2 kg.

The very low carbohydrate group lost 50% more fat than the conventional group, -2.2 kg vs -1.5 kg.

It should be noted that this is from a “poster presentation” at a conference, and as such has not been peer-reviewed.

What could be going on here? The extra fat loss was not a surprise to me. Low-carbohydrate diets have a much better record at fat loss than do conventional diets. However, this was not a weight-loss trial, and presumably the participants ate as much as they wanted.

How ketogenic diets could increase muscle gains

There are several ways that muscle gains could be greater when a ketogenic diet is combined with weight training.

  1. Adrenergic stimulation. Lower blood glucose (sugar) stimulates adrenaline release, which inhibits muscle protein breakdown. Although this doesn’t directly relate to gains, the breakdown of muscle is a normal, daily occurrence in healthy people, for instance with overnight fasting. Inhibiting this could mean greater gains.
  2. Ketone bodies produced by the VLCKD inhibit muscle breakdown. However, carbohydrate ingestion does this also, so perhaps this aspect is a wash.
  3. Growth hormone. Lower blood glucose means an increase in growth hormone. As carbohydrate does not increase growth hormone, this could be a major factor in better gains and fat loss.
  4. Dietary protein. Generally, people ingest more protein on a low-carb diet, resulting in increased muscle mass. However, the protein consumption here was the same in both groups.

Most bodybuilders will tell you that you need carbohydrates to build muscle, or that it’s more effective with carbohydrates, but there are several reasons for thinking that is not the case

Protein alone and not carbohydrate is responsible for muscle growth and, once the metabolism is adapted to burning fat, intense exercise can be performed on a low-carb diet.

One reason for thinking that carbohydrates make for better gains, and this may be a real consideration, is that people often spontaneously decrease calorie intake on a very low-carbohydrate diet. This may account for much of this diet’s efficacy in fat loss. But if you’re looking for those gains, you need to eat enough, and it could be that many low-carb eaters do not.

But it seems for most people a VLCKD could be just the ticket for muscle gains and fat loss when combined with regular resistance training.


Low Carb Best for health and weight loss

High-Fat Diet Doesn’t Cause Obesity

I wrote the other day about the less-than-optimal control animals and humans used in fasting and calorie-restriction studies. Partly this is due to the bad food that most people eat, as well as the substandard lab food that rats and mice eat. A similar problem exists in other diet experiments on lab animals. Here I’ll show that a high-fat diet doesn’t cause obesity – in lab animals anyway.

High-fat lab diets

If you read much of the scientific literature, you’ll come across lots of studies using lab rats and mice that were fed “high-fat” diets. Usually they produce ghastly results, like obesity, diabetes, cancer, cognitive deficits, and so on. Then the mainstream media trumpets these as meaning that you are going to get sick and die if you eat a high-fat diet.

Just to pull one more or less at random, “High-Fat Diet Disrupts Behavioral and Molecular Circadian Rhythms in Mice“. Control mice ate the Harlan Teklad 7012 diet of standard lab chow. It’s 25% protein, 17% fat, and 58% carbohydrate. Importantly, it contains no sugar and has high-quality, natural ingredients.

The high-fat group ate Research Diet 12451. Here are the ingredients:

This diet is 35% carbohydrate, 20% protein, and 45% fat. It contains sucrose – table sugar – as 17% of calories, as well as soybean oil, maltodextrin, and casein.

High fat? It’s more like dessert for rodents.

That amount of sugar is comparable to what the typical obese and heart-disease-prone American eats. Soybean oil has a high omega-6 content. Maltodextrin is a simple carbohydrate that turns to maltose and then glucose when absorbed, spiking blood sugar and insulin. Casein supplies all the protein, whereas the standard lab chow has no animal protein.

Yes, of course animals eating this garbage get sick.

Healthy high-fat diets

In contrast, look at another paper: A high-fat, ketogenic diet induces a unique metabolic state in mice. The animals on the ketogenic diet had lower body weight, lower glucose and insulin, and higher AMPK activity, a pro-longevity mechanism. When animals were switched to this diet, they lost weight. All very healthy, yet it was a high-fat diet, with 95% fat, 5% protein, and 0% carbohydrate. A very high-fat diet.

One of the experimental arms in this experiment was on the Research Diet 12451, as illustrated above. They got fat and sick.

Conclusion: Don’t believe everything you read

The animals on the “high-fat” diet in the first study were in reality eating a high-sugar, moderate-fat diet. Very misleading, if you ask me.

The animals in the second study ate a very high fat, no carb and sugar diet, and were healthy.

So next time you read about a high-fat diet making animals sick, diabetic, obese, or whatever, you can’t take it at face value.

Are carbohydrates needed to build muscle?

Lots of bodybuilders, most of them I would say, emphasize the need for a substantial amount of dietary carbohydrates to build muscle. The argument takes one or both of two forms; 1) that you need carbs to perform more intense exercise in the gym; and 2) carbs are needed to raise insulin and stimulate muscle growth. I’ve never found the arguments all that compelling, but then I’m just an average gym rat, not a bodybuilder extraordinaire. So how much truth is there in these statements?

First, as for intensity of workouts. A study was recently published in the Journal of the International Society of Sports Nutrition  – which looked at elite level gymnasts. After 30 days on a ketogenic diet, i.e one with a very low carbohydrate content, probably under 50 grams a day, the athletes’ strength and power had not diminished. However, even these elite athletes, who one would presume were already in terrific shape, lost about 2 kg of fat, with a “non-significant” increase in muscle. This shows that if anything, at least for gymnasts, who require a high level of strength, the ketogenic diet was better than their regular diets. The authors conclude:

Despite concerns of coaches and doctors about the possible detrimental effects of low carbohydrate diets on athletic performance and the well known importance of carbohydrates there are no data about VLCKD and strength performance. The undeniable and sudden effect of VLCKD on fat loss may be useful for those athletes who compete in sports based on weight class. We have demonstrated that using VLCKD for a relatively short time period (i.e. 30 days) can decrease body weight and body fat without negative effects on strength performance in high level athletes.

Assuming that the same holds for bodybuilders, let’s move on to muscle hypertrophy. Another recent study found that carbohydrate does not augment exercise-induced protein accretion versus protein alone. In this study there were two conditions: young men performed resistance training followed by ingestion of either 25 grams of whey protein, or 25 grams of whey plus 50 grams of carbohydrate (maltodextrin). Despite the fact that the extra carbohydrate raised blood glucose levels 17.5 times higher and insulin levels 5 times higher (that is, area under the curve) than protein alone, no difference was found in either muscle protein synthesis or muscle protein breakdown.

So as long as you get adequate protein, you’ve maximized the amount of hypertrophy you can get out of resistance training. Protein raises insulin, which is required for hypertrophy, but raising insulin further does nothing.

Finally there’s an interesting new study, one the co-authors of which is Jeff Volek, who’s done so much great work in this area. The effects of ketogenic dieting on skeletal muscle and fat mass. One reason why it’s interesting is that the men in the study were already resistance-trained. Normally in studies like this they like to use newbies, as you see greater results in them; if already trained subjects are used, and there’s a difference between groups, then you know it really worked well.

Twenty-six college aged resistance trained men volunteered to participate in this study and were divided into VLCKD (5 % CHO, 75 % Fat, 20 % Pro) or a traditional western diet (55 % CHO, 25 % fat, 20 % pro). All subjects participated in a periodized resistance-training program three times per week….

Results: the ketogenic diet group gained 4.3 kg lean mass (muscle) compared to only 2.2 kg for the traditional diet group; the ketogenic group lost 2.2 kg of fat, compared to 1.5 kg in the traditional group.

I’d say this last study puts to rest any argument for lots of carbohydrates in weightlifting. The very low carbohydrate ketogenic diet was superior to a diet with 55% carbohydrate. Note that protein percent was the same for both groups.

Finally, there’s a very good book I recommend by the above-mentioned Jeff Volek and co-author Stephen Phinney, The Art and Science of Low Carbohydrate Performance.

So, no, carbohydrates are not needed to build muscle, and in fact muscle building might be even better without them.



Low-Carbohydrate Diet Beats Others for Weight Loss



Low-carbohydrate food pyramid.

Low-carbohydrate food pyramid.

Weight loss and the myth of saturated fat


What’s the best diet for weight loss? Much controversy swirls around this question because although diets like the low-carb Atkins diet have had great success, we don’t know whether they’re more effective, and besides we’ve been told for years that too much saturated fat in the diet may be bad for our health.

The “fact” that saturated fat may cause heart disease and be bad for our health generally has finally, and I believe definitively, been shown to be a myth. A meta-analysis from a few years ago, one of whose co-authors was Dr. Ronald Krauss, than whom it would be impossible to be more mainstream, showed that “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD [cardiovascular disease].” The myth of dietary fat and health risks has been expounded upon at length in the recent book by Nina Teicholz, The Big Fat Surprise, which I highly recommend.

As the myth of saturated fat has been debunked, we’re left with which diets are better for weight loss. One factor in that analysis is compliance, that is, to what extent dieters will stay on a diet. In compliance, there are basically two things to consider: 1) whether the food taste good; and 2) whether hunger can be kept under control.

Diets must control hunger


Food doesn’t just supply us with nutrients; it’s pleasant and the occasion for social interaction, and a diet depriving people of these will generally make them unhappy and unwilling to continue.

And if dieters are hungry, they are much more likely to break their diets and revert to their old, weight-gaining ways.

Low-fat diets, the kind prescribed over the past few decades, generally deprive dieters of foods that humans find naturally satisfying and that taste good, fatty foods like steak and all kinds of meats, butter, cream, cheese, eggs, even olive oil. Many or most people find that they feel deprived on such a diet – I would anyway.

On the other hand, low-carbohydrate diets deprive dieters of or severely limit sugar, bread, rolls, pasta, tortillas, candy, pastries, and any number of other things. However, on a calorically restricted low-fat diet, you can’t really eat your fill of these foods either.

So, as far as taste goes, a low-carbohydrate diet would seem to offer a better choice, being able to eat one’s fill of “main meal” type, satisfying foods, while limiting anything made with flour or sugar. Low-fat diets, if calorically restricted, limit these foods anyway.

What about hunger? Most people report less hunger on a low-carbohydrate diet, so they’re more likely to stay on it. But the kicker is that most low-carbohydrate diets do not restrict calories, while low-fat or conventional diets do. So even if low-carbohydrate, high-fat foods didn’t satisfy hunger more, the fact that one can just eat more of them would seem to make up for it. But all the evidence points to low-carb, high-fat foods as better able to eliminate hunger – in fact, that’s part of the mechanism that makes them work.


A head-to-head comparison of low-carbohydrate, low-fat, and Mediterranean diets


A study from a few years ago directly compared three different diets for weight loss: Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. (New England Journal of Medicine.)

The low-fat diet was calorically restricted, with a target 1800 calories a day for men, 1500 for women. (Editorial comment: I’d be hungry on that amount of calories.) It was 30% of calories from fat, and “participants were counseled to consume low-fat grains, vegetables, fruits, and legumes and to limit their consumption of additional fats, sweets, and high-fat snacks”. (Editorial comment: even on this diet, sweets are limited.)

The Mediterranean diet’s target calorie intake was the same as for the low-fat, but with a goal of 35% calories from fat, “the main sources of added fat were 30 to 45 g of olive oil and a handful of nuts (five to seven nuts, that’s it).

The low-carbohydrate diet was not restricted in calories; it was all you can eat. (Now we’re talking.) It provided “20 g of carbohydrates per day for the 2-month induction phase…, with a gradual increase to a maximum of 120 g per day to maintain the weight loss. The intakes of total calories, protein, and fat were not limited. However, the participants were counseled to choose vegetarian sources of fat and protein and to avoid trans fat. The diet was based on the Atkins diet.” Unfortunately, we see the fear of saturated fat loom here, with “vegetarian sources of fat and protein”. At the beginning, the diet amounts to a ketogenic diet; it’s unclear why they felt the need to increase carbohydrates from the original to 120 grams. Possibly they think better compliance would result.

The study lasted for 2 years; all participants were either overweight (BMI ≥27), or with diabetes or coronary heart disease.

So, what happened? Drum roll, please…

Weight loss on low-carbohydrate, low-fat, and Mediterranean diets. Low-carb for the win.


Low-carbohydrate diet resulted in more weight loss


For participants who completed the entire 24-month program, weight loss was 3.3 kg (7.3 lbs.) on low-fat, 4.6 kg (10.1 lbs.) on the Mediterranean diet, and 5.5 kg (12.1 lbs.) on the low-carbohydrate diet. Low-carb was the clear winner.

Note from the above graph that with all diets, most weight loss occurred in the first 6 months, with either a plateau (Mediterranean) or a gradual weight regain. This pattern is often seen in diet studies and, no doubt, in real-world dieters.

The reasons for that are at least two or three. One is that dieters lose their initial enthusiasm and start to cheat. Another is a decrease in metabolism that follows weight loss; although this occurs with all weight loss, the low-carbohydrate diet appears to have a better record of maintaining metabolism, one reason being that it’s not calorically restricted. Finally, the low-carb diet had “cheating” built into it, with a beginning carbohydrate allocation of 20 grams a day, but rising to 120 grams a day later. That alone could easily account for weight regain.

The low-carbohydrate diet reduced disease risk more


The researchers wanted to know how each of these diets affected heart disease risk, and thus looked at lipid profiles. Results below.

The low-carbohydrate diet had the best lipid profile results.

We know that in lipid profiles, triglycerides (lower is better), HDL cholesterol (higher is better), and the ratio between the two have the most significance for heart disease risk. The low-carbohydrate diet trounced the others in this category.

Fasting glucose (chart not shown) remained about the same for all groups, although in diabetics, the Mediterranean diet group showed the greatest improvement.

Also in non-diabetics, the low-carbohydrate group showed the greatest decrease in fasting insulin levels. Since insulin is a pro-growth, anabolic hormone, and is implicated in aging, this gives further backing to the fact that a low-carbohydrate diet is an anti-aging diet. Of great interest, the level of C-reactive protein, which is a measure of inflammation, dropped the most on the low-carb diet. Again, since increasing inflammation is associated with aging, the low-carb diet can potentially slow the aging process.

The results show that the low-carbohydrate diet was the clear winner for weight loss. (Diabetics had somewhat better results with the Mediterranean diet, although not for weight loss.)

The better results on low-carb were likely due to two things, in my opinion. One is that insulin levels dropped. Insulin helps drive fat into cells, and lower insulin levels allow fat cells to release fat to be burned. The other reason is probably better compliance. This low-carbohydrate diet was unrestricted in calories, i.e. all-you-can-eat, therefore the participants on this diet were unlikely to get hungry and grab the nearest food available. The participants on the other, calorically restricted diets may have been much more likely to get hungry and cheat.

If weight loss is your goal, the choice seems clear enough. The addition of weight training and adequate protein intake to a low-carb diet will make the retention and even gaining of muscle possible, even while losing fat. (Annals of Nutrition and Metabolism.)

A couple of books that I like that thoroughly explain the low-carbohydrate diet, both by the same authors, Jeff Volek and Stephen Phinney, are The Art and Science of Low Carbohydrate Living, and for athletes, The Art and Science of Low Carbohydrate Performance.



Why a Low-Carb Diet Is Best for Weight Loss

If you want to lose weight, you have a number of choices. The most popular is to cut calories and eat a low-fat diet. A way that’s becoming more popular, because it works much better, is to cut carbohydrates. Here we’ll take a look at scientific proof that a low-carb diet is best for weight loss.

No calorie counting

The biggest impediment to losing weight on a low-calorie diet is hunger. If you voluntarily reduce calories while eating the same foods, you get hungry, as is to be expected. Your body defends its weight, i.e. it has a set point, and makes you hungry if your weight moves away from the set point.

On a low-carbohydrate diet, you merely cut the amount of carbohydrates in the diet, and in most studies looking at low-carb diets, the dieters ate as much as they wanted. Only carbohydrates were restricted. Cutting carbohydrates lowers levels of the hormone insulin, which signals the body to store fat, and which is responsible for setting the body weight set point. The result is nearly effortless weight loss.

In the first study we’ll look at, a group of obese women were randomized to either a low-fat, low-calorie diet, or a low-carbohydrate diet that was not restricted in calories, and followed for 6 months. Weight loss result in the chart below.

low carb weight loss

The low-carb group ate 20 g of carbohydrate daily, but were allowed to increase this to 40 to 60 g after 2 weeks, so long as they remained in ketosis as shown by urinary testing. The low-fat group was restricted in calories by 30% and ate about 55% of their calories as carbohydrates.

Despite the fact that the low-carb group could eat as much as they wanted, they spontaneously reduced their calorie intake to about the same as the low-fat group. That shows the power of low-carb in reducing hunger and changing the body’s weight set point. And they still lost more weight, an average of 7.6 kg, than the low-fat group, at an average of 4.2 kg.

You can even eat more calories and still lose weight

The second study concerns weight loss in obese teenagers. A group of adolescents, average age 14, were assigned to either a low-carb diet or a low-fat diet.

The low-carb group was instructed to keep carbohydrates at less than 20 g a day for the first 2 weeks, but increasing to 40 g a day in weeks 3 through 12. They could eat as musch as they wanted.

The low-fat group was instructed to keep fat at <40 g a day. They also could eat as much as they wanted.

Here are the results.

low carb weight loss 2

The low-carb teenagers averaged 9.9 kg of weight loss, compared to 4.9 kg in the low fat group. (That’s 22 pounds vs 11 pounds.) That was despite the fact that the low-carb group ate over 1800 calories a day, while the low-fat group ate 1100 calories a day. That’s the power of lowering carbohydrate intake. Also it’s guaranteed that the low-carb group was less hungry.

You don’t even need to reduce carbohydrates much

The third study compared a low-carbohydrate to a low-fat diet in severe obesity. These people had a high prevalence diabetes or metabolic syndrome.

The low-carbohydrate group was instructed to keep carbs at <30 g a day. However, they didn’t. They could eat as much as they wanted.

The low-fat group was instructed to keep fat  at <30% of calories, and to reduce their calorie intake by 30%.

low carb weight loss 3

The low-carb group lost 5.8 kg after 6 months, the low-fat group 1.9 kg. (13 pounds vs 4 pounds.) The low-carb group spontaneously reduced their calorie intake, so that the 2 groups ate about the same number of calories, again showing the power of reducing hunger and body weight set point.

Notably, the low-carb group wasn’t very compliant, and they only reduced their carb intake to 37% of calories at 6 months, vs 51% for the low-fat group. Yet they still lost more weight.

Low-carb vs low fat and Mediterranean diets

The fourth study was a three-way comparison between a low-carb, low-fat, and Mediterranean diets. The low-fat and Mediterranean diets were restricted in calories, with limits of 1500 calories daily for women, and 1800 for men.

The low-carb dieters could eat as much as they wanted, so long as they restricted carbohydrates to 20 grams daily initially, but increasing to a maximum of 120 grams.

Here’s what happened:

low carb weight loss 4

Once again, low-carb is a clear winner. Low-fat lost 2.9 kg, Mediterranean 4.4 kg, and low-carb 4.7 kg. The low-carb group still ate a whopping 40% of calories as carbohydrates, although that was down from 51% at baseline, representing a drop of 120 grams of carbs daily.

Noteworthy is the increase in weight after the first few months of weight loss, which was greatest in the low-carb group. That group actually increased its carb intake slightly. Another explanation might be a lower metabolic rate and/or less exercise. the low-carb group did decrease the amount of exercise between 6 and 24 months; the low-fat group increased exercise.

Reviews of low-carb diets

We’ve seen above that several studies have found that low-carbohydrate diets are superior for weight loss. have I cherry-picked the studies? Nope.

Several meta-analyses (reviews of studies) have found that low-carb diets beat calorie-restricted low-fat diets.

Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis. This study concluded:

This trial-level meta-analysis of randomized controlled trials comparing LoCHO diets with LoFAT diets in strictly adherent populations demonstrates that each diet was associated with significant weight loss and reduction in predicted risk of ASCVD events. However, LoCHO diet was associated with modest but significantly greater improvements in weight loss and predicted ASCVD risk in studies from 8 weeks to 24 months in duration. These results suggest that future evaluations of dietary guidelines should consider low carbohydrate diets as effective and safe intervention for weight management in the overweight and obese, although long-term effects require further investigation.

Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. This study concluded:

Compared with participants on LF diets, participants on LC diets experienced a greater reduction in body weight.

What to eat on a low-carb diet

Low-carb diets vary in the degree of carbohydrate restriction. One scheme that I used in my book Stop the Clock was the following:

  • moderately low-carb: <130 grams of carbohydrate daily
  • low-carb: 50 to <130 grams daily
  • very low-carb ketogenic: <50 grams daily.

As we saw in this article, virtually any degree of carbohydrate restriction is beneficial. But, the more you restrict carbs, the better your weight loss is likely to be.

Timothy Noakes, M.D., a noted advocate of low-carb diets, recently published an article, Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review. In it, he listed the following foods as being “green-lighted” for a low-carbohydrate diet:


This list is meant for people who are insulin-resistant. If trying to lose weight, it would be a good idea to go easy on the added oils and nuts.

You should omit the following foods entirely:

  • anything made with flour: bread, pasta, tortillas, pastries
  • anything with added sugar: soft drinks, fruit juice, candy, cookies
  • starch: potatoes, sweet potatoes

Did I miss anything? It’s easy, just eat plenty of meat, eggs, vegetables, cheese. Don’t go hungry.

For what it’s worth, I eat this way all the time. Most days my carb intake is probably 20 to 60 grams, some days rising to 100.