Some Facts About Seaweed That You Must Know

 

Japanese cuisine is one of the most famous and favorite kind in the whole world. Sushi, ramen, maki, gyudon…The list of amazing Japanese food is endless. And one of their staple ingredients is seaweed. It’s actually a common name for a number of species of marine plants and algae. They usually grow in oceans, but they also thrive in lakes, rivers, and other water bodies.

All kinds of seaweed are edible, though some taste better than others. Also, some can lead to an upset stomach.

For years the Japanese have been using this unlikely plant life in their food. Plenty like snacking on dried seaweed straight out of the bag. You can also make use of it in a salad, in soups, or sprinkled on other food.

Most seawood available don’t taste bitter. There are even some types that taste sweet, and even others with umami flavors. This means it’ll be easier to introduce to picky eaters.

Types of Seaweed

The different categories of seaweed available are made based on their cell structure, pigments, and other factors. The most common types are the following:

Blue-green algae. These include chlorella and spirulina.

Green algae. Some examples are sea grapes, ulva, or sea lettuce.

Brown algae. Belonging in this category are kelp, kombu, arame, and wakame (the one used in miso soup)

Red algae. Examples are laver, nori, and dulse.

Its Nutrient Content

I know it may not look like much, and some people actually shudder at the thought of eating it, but seaweed is very healthy for you. It’s known to be chock-full of vitamins, minerals, and plenty other nutrients. In fact, it’s much more nutrient-dense as compared to vegetables that grow on land.

For one, seaweed is known to have high amounts of the fat-soluble vitamin K. It also possesses a good amount of iron as well as calcium. And finally, this plant food is high in iodine as well.

On top of that, seaweed contains plenty of other nutrients. It has fiber, prebiotics, omega-3 fatty acids, and antioxidants. It has vitamins A, C, D, E, and the B vitamins. For its mineral content, it boasts of magnesium, potassium, and copper.

 

It’s been said that one of the secrets of the Japanese for living long and healthy lives is their consumption of seaweed. Here are a few of the benefits this helpful algae boasts that you can enjoy for yourself.

Combats Cancer

There are certain types of seaweed with anti-carcinogenic properties. They have compounds that effectively activates the process of natural cell death among lymphoma, leukemia, colorectal, and stomach tumor cells.

Other types of seaweed have the ability to decrease estrogen levels, which in turn reduce the risk of breast cancer. The soluble fiber in seaweed is also effective in reducing the likelihood of colon cancer.

Boosts Heart Health

Certain compounds found in seaweed work together to ensure your heart will keep on pumping for a long time. The sulfated polysaccharides it has reduces blood pressure and prevents blood clotting. They also reduce LDL cholesterol and total cholesterol levels, as well as lower high blood pressure.

Prevents Diabetes

Adding seaweed to your daily diet helps in reducing your risk of developing diabetes. It contains compounds that reduces insulin resistance and stabilizes blood sugar levels. The type of fiber the water plant has actually slows down the speed at which carbohydrates are absorbed in the body. This makes int infinitely easier for your body to stabilize blood sugar levels.

Aids in Weight Loss

Seaweed has fiber, which increases the feeling of satiety and enhances the feeling of fullness, all while keeping hunger pangs at bay.

It also contains fucoidan, which enhances the breakdown of fat and prevents its formation. And finally, it has a low calorie content, which makes it a healthier option as an afternoon snack.

All these work together to achieve healthy and effective weight loss.

Boosts Gut Health

Bet many of you didn’t know that seaweed can do wonders to your digestion. Well, it does. And here are the numerous ways how.

First, since it’s rich in fiber, it makes sure you have regular bowel movements. This prevents constipation and ensures smooth digestion.

Second, the prebiotics found in seaweed improve the production of healthy bacteria in the gut and. They also reduce the amount of harmful bacteria in the gut more effectively than other types of prebiotics. In addition, these prebiotics prevent the formation of stomach ulcers by blocking harmful bacteria from sticking to the gut wall.

Provides Better Skin

Plants from under the sea can do so much for our skin. From cleansing, to toning, to moisturizing, to revitalizing, to repairing…I could go on. That’s why so many beauty products make use of the different types of seaweed.

It contains antioxidants, which provides anti-aging properties. Say goodbye to wrinkles, fine lines, dark spots, saggy skin, and other skin blemishes. And according to Dr. Max Huber, the founder and creator of Crème de la Mer, “it is a powerful catalyst for skin renewal, bathing the skin in moisture and calming sensitivities.”

Seaweed can also be applied topically. In this process, it can draw excess fluid and waste products from the skin. It also cleanses dead skin cells and other skin impurities on the surface.

Guarantees Hair Health

Numerous extracts in seaweed help hair to rebuild itself and makes it grow stronger. They promote scalp hydration, which then improves the condition of dry hair. They also increase hair mineralization, which thickens hair. And finally, they have the ability to protect the hair from environmental damage.

Ensures a Healthy Thyroid

The thyroid is a gland in your neck that helps produce and regulate hormones. It also makes sure your metabolism is functioning well. If your thyroid is not working properly, this will lead to a multitude of effects, like high cholesterol, fatigue, and muscle weakness. If left untreated, this will then develop to even more serious medical issues, such as goiters, memory loss, and heart palpitations.

That’s why maintaining healthy levels of iodine in the body is so very important. And that’s where seaweed comes in.

Word of Warning

Though eating seaweed is generally considered safe, there are still some side effects you need to watch out for.

Contains Heavy Metals

There are some varieties of seaweed that contain high levels of arsenic, mercury, lead, or cadmium. Note that the FDA regulates the levels of these heavy metals in fresh seawood. Unfortunately, supplements are not regulated and may possess levels that could be dangerous to your health.

Also read our latest article: the hype about garcinia cambogia.

Types of seaweed to watch out for include hijiki (contains arsenic well above the safety limit), laver, gulfweed, sea mustard, and seatangle.

Causes Gastrointestinal Issues

Some people may experience mild to moderate gastrointestinal issues when taking seaweed. According to a 2012 study in The American Journal of Clinical Nutrition, a few individuals experience nausea, abdominal pain, bloating, and diarrhea.

Interferes with Kidney Function and Blood Thinners

There are some types of seaweed that have very high levels of potassium and sodium. Too much of the two minerals can cause trouble with the kidneys.

Also, since it’s known to have high levels of vitamin K as well, this could interfere with blood-thinning medications. Individuals who are taking blood thinners should always check with their doctors before taking in seaweed.

ALSO: What do you know about nad+ and weight loss probiotic , are these products really good for your health?

A Healthier and Happier Way to Start Your Day

 

Do you often find yourself rolling off the bed in a messy heap and sluggishly shuffling your feet to the bathroom every morning? And this is true even when you actually had a solid 8 hours of sleep (in the effort to be healthy) the night before! Meanwhile, there are others who are often remarkably bright-eyed, instantly perky, and amazingly wide awake… ready to tackle problems and take on the world as soon as they open their eyes.

Are you green with envy just thinking about it?

Well, what if I share an amazing secret with you? One that will amazingly transform your mornings and provide you with incredible energy to last you the entire day! Best of all, it won’t cost you much time and effort to prepare. Interested? I bet, you are!

Before I reveal that sensational secret, however, let’s first discuss the real reasons behind that uncontrollable lethargy you often get in the mornings.

While You Were Sleeping: The Unvarnished Truth

Do you know that while you’re catching some Zs, your body loses a ton of essential nutrients? This is because even when you’re at rest, your body and brain are technically still up and about. Important basic bodily functions such as your cardiovascular, digestive, and respiratory systems continue to operate.

Not to mention that there’s also the production of growth hormones that renew tissues, stimulate collagen growth, and build muscles in your body. All of these activities use up stored energy as well as vitamins and minerals in your body, which means by the time you wake up, all those mentioned resources in your body have been depleted. And that’s the reason for your slow movements, feelings of listlessness, and general lack of energy in the morning.

And no, eating the usual cereal, pancakes, oatmeal, toast, or whatever breakfast you typically have is not enough. If you think they can provide you sufficient energy and complete nutrients for the day (or even just the morning), you are sorely mistaken.

These kinds of meals will most likely only provide you with carbs and protein, maybe a little bit of fiber (sometimes, if you’re lucky). However, the human body is a complex machine that needs not only those previously mentioned nourishment but also a bunch of other essential micronutrients… such as enzymes, probiotics, phytonutrients, antioxidants as well as a long list of vitamins and minerals.

What’s worse is before you know it, that short-lived smidgen of energy you experience after breakfast unexpectedly fizzles out, and the curse of the legendary lethargy comes back with a vengeance.

The Scourge of Seconds

Not all breakfasts are created equal. And that is why another unfortunate issue of hastily prepared and eaten breakfasts is its low satiety index. This means that if you consume foods that don’t have enough essential nutrients to tide your over until the next meal, you will more likely end up hunting for and wolfing down a second helping.

Why?

Because hunger pangs are quite impossible to resist, that’s why! Just try ignoring those growling noises your stomach makes and you will get more trouble than you bargained for. Believe you me, you’ll end up munching on anything you can get your hands on, which could be another sandwich, more toasts, or some half breakfast-half lunch some people like to call “brunch”.

You may even find your hands reaching for those Snickers bars you spied on your co-worker’s desk of their own accord. Quite an embarrassing thought, right? Well, your hunger pangs don’t really care.

So instead of eating just one meal in the morning, you actually end up devouring two or several meals before lunch. Goodbye good health, hello carbs overload (and not much else). Yikes!

And remember, your body needs way more than that to be in tip top shape and be able to function efficiently throughout the day.

Super Breakfast: The Real Deal

Now’s the time to let you in on that awesome secret. There’s an amazingly brand-new superfood formula that is exactly what you need every morning. Take it from us, Life Essentials has all the ingredients to supply the rest of your essential dietary needs and help you efficiently jump-start your day right.

Moreover, it’s a 100% USDA-certified organic drink that can provide your body with all the vital nutrients it needs, but may not be getting. We’re talking about antioxidants, enzymes, fibers, probiotics, vitamins, minerals, phytonutrients, and plenty more. As a matter of fact, each scoop of Life Essentials has an ORAC value that’s equivalent to 2 servings of nutritious vegetables. Amazing, right?

All these nutrients work together to give your body all the energy it requires to face the day ahead. Move faster. Think quicker. Feel stronger. Be better and healthier.

It’s a perfect complement to your favorite breakfast. Simply add 1 scoop of Life Essentials powder into a tall glass of water and stir well. Drink it with any of your favorite breakfast foods. Et voila, you’re ready to go!

Feel energized and invigorated—a fabulously revamped version of yourself.

So start your day the healthier way with Life Essentials.

You can take Apple Cider Vinegar or garcinia cambogia to stay fit and to give more strength to your immune system add cumin to your daily diet.

Type of Fat you consume matter where it ends up

The role of dietary fat in body fat distribution is not well known.

However, some interesting results from the LIPOGAIN study were published in the July, 2014 issue of Diabetes.

This study compared the effects of overfeeding saturated and polyunsaturated fat on fat accumulation and body composition.

Here is a detailed summary of the findings.

BACKGROUND

Visceral fat accumulates in the abdominal cavity, around organs such as the intestines, liver and pancreas.

Conversely, ectopic fat accumulates inside the organs themselves, mainly the liver and pancreas.

Both visceral and ectopic fat are associated with an increased risk of chronic disease, such as heart disease and type 2 diabetes.

Combined, the adverse health consequences of visceral and ectopic fat are known as metabolic syndrome. For this reason, well-designed research on the causes of visceral and ectopic fat is extremely valuable.

STUDY REVIEWED

A team of Swedish scientists set out to investigate the effects of eating high amounts of saturated fat and polyunsaturated fat on body composition and the accumulation of visceral and ectopic fat.

Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans.

BASIC STUDY DESIGN

This was a 7-week, double-blind, randomized, parallel-group trial in 39 young and normal-weight men and women.

The purpose of the study was to compare the effects of eating high amounts of either saturated fat or polyunsaturated fat.

Participants were randomly assigned to one of two groups:

  • Saturated fat group: Participants were overfed with muffins high in saturated fat for 7 weeks. The fat was in the form of refined palm oil, which is rich in palmitic acid, the most common saturated fat in the modern diet.
  • Polyunsaturated fat group: Participants were overfed with muffins high in omega-6 polyunsaturated fat for 7 weeks. The fat was in the form of refined sunflower oil, which is rich in linoleic acid.

The amount of muffins was adjusted so that each participant would achieve a 3% weight gain during the study period.

On average, the daily amount of oil added to the muffins was about 40 grams, and the calorie excess was 750 kcal per day.

The researchers measured total body fat, visceral fat, abdominal skin fat, liver fat, pancreatic fat and lean tissue.

Bottom Line: This study was a randomized controlled trial in healthy, normal-weight individuals. It compared the effects of overeating palm oil and sunflower oil on fat accumulation and body composition.

FINDING 1: FAT MASS AND LEAN MASS GAIN WERE AFFECTED

Participants in both groups gained equal amounts of weight, or 1.6 kg (3.5 lbs).

However, those who were fed saturated fat gained significantly more fat mass, whereas polyunsaturated fat led to a greater increase in lean mass.

In fact, the ratios of lean and fat tissue gain in the polyunsaturated and saturated fat groups were approximately 1:1 and 1:4, respectively.

The chart below shows changes in fat mass and lean mass in both groups.

This difference remained, even when total body water content was taken into account.

These findings are supported by previous studies, one in postmenopausal women and one in rats.

However, exactly how this works is unknown. It is also unclear what the current study’s increase in lean tissue actually represents or signifies.

Bottom Line: Eating high amounts of saturated fat caused more fat accumulation than eating polyunsaturated fat. Additionally, polyunsaturated fat appeared to cause a greater increase in lean mass.

FINDING 2: SATURATED FAT CAUSED MORE VISCERAL FAT GAIN

There are two types of belly fat:

  • Subcutaneous: This type of belly fat is stored directly underneath the skin.
  • Visceral: This type of belly fat is stored inside the abdominal cavity, surrounding the intestines, liver and pancreas.

Visceral fat is much more harmful than subcutaneous fat, and is associated with various chronic diseases.

In the present study, participants who were fed saturated fat gained significantly more visceral fat, compared with those who got polyunsaturated fat. In fact, the difference was nearly two-fold.

The chart below shows the differences in visceral fat changes between groups.

These results suggest that overeating polyunsaturated fat may cause less fat accumulation in the abdominal cavity, compared to saturated fat.

That being said, overeating is still unhealthy, no matter what you are eating — overeating polyunsaturated fat just seems to be less bad.

Bottom Line: Eating high amounts of saturated fat from palm oil caused more visceral fat accumulation than eating polyunsaturated fat from sunflower oil.

FINDING 3: SATURATED FAT CAUSED MORE LIVER FAT GAIN

Participants who were overfed with saturated fat gained significantly more liver fat than those who ate polyunsaturated fat.

The chart below shows the differences in liver fat changes between groups.

These results are well supported by several other studies.

Observational studies have found high dietary intake of saturated fats, and low intake of polyunsaturated fats, to be associated with increased liver fat.

Fatty livers also contain low levels of polyunsaturated fat. Additionally, a clinical trial found that the polyunsaturated fat in sunflower oil reduced liver fat, compared to a diet rich in saturated fat.

Accumulation of liver fat may lead to an adverse condition known as non-alcoholic fatty liver disease (NFLD). NFLD is present in up to 75% of obese people.

Fatty liver is believed to contribute to the development of many chronic diseases, such as type 2 diabetes and metabolic syndrome.

Bottom Line: Eating high amounts of saturated fat from palm oil caused greater liver fat accumulation than eating polyunsaturated fat.

FINDING 4: PANCREATIC FAT DECREASED IN BOTH GROUPS

On average, pancreatic fat decreased by 31%. There was no significant difference between groups.

This unexpected finding cannot be explained based on the study’s results, and needs to be confirmed by other studies before any solid conclusions can be reached.

Bottom Line: Pancreatic fat decreased significantly in both groups. The finding needs to be confirmed in other studies before any conclusions can be made.

LIMITATIONS

This high-quality study appears to be well-designed and executed. Nevertheless, there are several limitations worth mentioning.

SUNFLOWER OIL CONTAINS MORE VITAMIN E

Sunflower oil contains more vitamin E than palm oil, and vitamin E may reduce liver fat. However, the amount of vitamin E in the sunflower oil was probably too low to have any significant effects.

THE RESULTS MAY NOT BE GENERALIZED

The study tested palm oil and sunflower oil, and may not be generalized to all saturated or polyunsaturated fatty acids.

OTHER NUTRIENTS MAY PLAY A ROLE

The dietary context may play an important role in how the body reacts to high amounts of fat.

The muffins provided to participants were also high in fructose and refined carbs, which could have affected the findings.

THE STUDY EXAMINED ONLY LEAN INDIVIDUALS

All study participants were lean, so the results may not apply to obese or diabetic individuals.

Bottom Line: The study was well designed and executed. There are a few limitations, so the results should not be generalized.

SUMMARY AND REAL-LIFE APPLICATION

This study shows that dietary fat type may affect fat distribution and body composition.

To summarize the findings:

  • High amounts of palm oil (palmitic acid) led to greater liver and visceral fat gain, compared to sunflower oil.
  • High amounts of sunflower oil (linoleic acid) led to almost a three times greater increase in lean body mass, compared to palm oil.

Simply put, palm oil caused fat accumulation in places associated with adverse health outcomes. Conversely, sunflowers oil caused less fat gain overall and much greater gain in lean mass.

These results are of limited value for health-conscious consumers, since they may only apply to those that are overeating and gaining weight. However, a previous study showed a similar effect during a weight-maintenance diet.

That being said, this doesn’t necessarily mean that saturated fat is unhealthy, only that eating too much of it may have worse consequences compared to eating an equal amount of polyunsaturated fat. At least in the context of a high-calorie diet.

You can take something like Apple Cider Vinegar
, or garcinia cambogia
, but at the end of the day, how many carbs
you eat makes a difference if you want to lose weight fast.

Cancer a Mitochondrial Disease – Keto diet and NAD+ therapy

This theory of cancer is more than 100 years old, but it didn’t become the dominant view until the 1950s, when, after Watson and Crick, genes assumed an exalted position in the study of biology.  The “somatic mutation theory” continues to dictate the course of cancer research and treatment today.

It is uncontested that cancer cells have abnormal chromosomes.  Dozens of different mutations have been found in malignant cells.  They have been catalogued as different oncogenes, and because they are so different in their functions, cancer has been re-conceived from a single disease to a category containing many different diseases with similar symptoms.

Are mutated genes the root cause of cancer?  Toxins that commonly break DNA (teratogens) are also found to cause cancer (carcinogens).  Radiation, ditto.  “Ionizing” radiation packs enough wallop in each photon to break a chemical bond, and is associated with cancer, while non-ionizing radiation (visible, infrared, and radio waves) is not mutagenic and generally not carcinogenic*.  This has been taken as powerful circumstantial evidence for the prevailing theory.

A direct answer to the question of whether cancer originates in the nuclear DNA is available from an experiment that is simple in principle: Swap nuclei between two cells, one normal and one malignant.  Take the mutated DNA out of a cancer cell and put it in a normal cell, to see if it becomes malignant.  Take the un-mutated DNA out of a normal cell and put it in a cancer cell to see if the cell is rescued and restored to health.

This experiment has been technically feasible for more than 30 years, and indeed Barbara Israel and Warren Schaeffer actually performed both experiments at UVM and wrote them up in 1987 [ref, ref].  The results were exactly the opposite of what was expected: The cell with normal cytoplasm and cancerous nucleus was normal; the cell with normal nucleus and cancerous cytoplasm was cancerous.

This result has been confirmed in other labs[reviewed by Seyfried, 2015].  Still, the genetic paradigm has a stubborn grip on cancer research and treatment to this day.

An alternative theory of cancer as a metabolic disease was put forth by the Nobel polymath Otto Warburg in the 1930s.  The principal proponent of this theory today is Thomas Seyfried of Boston College.  Seyfried cites evidence that damage to the nuclear DNA, conventionally thought to be a root cause of cancer, is actually an effect of the damaged mitochondria and irregular metabolism.  “The metabolic waste products of fermentation can destabilize the morphogenetic field of the tumor microenvironment thus contributing to inflammation, angiogenesis and progression.”

 

Respiration and Fermentation

Every cell in our bodies (and almost every cell in all eukaryotes everywhere) makes uses of energy in the form of ATP, adenosine triphosphate.  ATP is manufactured in the mitochondria, usually by a controlled burning of sugar to form CO2 and H2O.

Highly energy-intensive cells such as muscles and nerves have thousands of mitochondria in each cell.  The word “respiration” in this context is used to mean burning sugar in an efficient energy conversion process, yielding 38 ATPs for every sugar molecule.

But when oxygen is scarce, perhaps because you’re breathing as fast as you can or sprinting in deep anaerobic mode, another process can be used to rapidly convert available sugar stock to lactic acid, requiring no oxygen at all, but yielding only 2 ATPs per sugar molecule.  The latter process is called “fermentation”.  (This observation explains the extraordinary effectiveness of interval training (sprints) for weight loss.)

Warburg was among the first to notice [1931] that most cancer cells use fermentation rather than respiration as an energy source.  Metabolic studies pointed to damaged mitochondria in tumor cells that had become inefficient in producing sufficient energy through respiration.

He theorized that impaired mitochondrial function is the root cause of cancer.  In fact, Warburg did some of the early work establishing the role of mitochondria as cellular energy factories.

So most cancer cells are sugar addicts.  They consume enormous amounts of sugar, both because they are actively growing and dividing, and also because they use sugar so much less efficiently than normal cells.  A PET scan can be used to visualize concentrations of sugar in the body, and PET technology is often used to locate tumors.

Sugar is easily made from carbohydrate foods, and when you eat a diet containing carbs, sugar is the fuel of choice.  Ketones are an alternative fuel used by the body when burning fat, either stored fat or ingested animal fat or vegetable oils.  (Medium chain saturated fatty acids like coconut oil seem to be most effective in inducing metabolic ketosis.)  Unlike sugar, ketone bodies cannot be fermented.  They generate ATP energy only through oxidative respiration in the mitochondria.

The logical question:

Are zero-carb diets an effective treatment for cancer?

Some well-known cancer drugs (Gleevec, Herceptin) already target the fermentation metabolism.  Acarbose has been proposed but not yet tried.  But might it be safer and more effective to starve cancer cells by cutting carbohydrates in the diet to zero?  There is a robust literature suggesting, “yes” [e.g., ref, ref, ref, ref, ref, ref, ref] but so far the results have been less than earth-shaking.

A search of ClinicalTrials.gov yields 25 trials of ketogenic diet variants for cancer treatment.

Most are in early stages, 5 have been completed, 2 have results.  In this study, the ketogenic diet, with or without chemotherapy, did not cure glioma.  This small study found modest benefits in a variety of advanced cancers.

These results are consistent with many mouse studies, in which some benefit was recorded from the ketogenic diet, but not a dramatic difference.  The most encouraging results I have found was a study in which 9 of 11 mice treated with a combination of radiation and a ketogenic diet were cured of brain cancer.

Clearly, this is no miracle cure, but it’s too early to give up–we’re just figuring out how to make the diet work, and it has not yet been tried except at late stages, after all else has failed.

Fasting shows more promise than ketogenic diets.  (Perhaps fasting lowers blood sugar even more than ketogenic diets.)  A series of studies by Valter Longo make the case that fasting simultaneously sensitizes cancer cells to chemo or radiation and de-sensitizes normal cells.

Seyfried has proposed a “press-pulse” system based on this vulnerability, targeting the glucose metabolism and the glutamine metabolism with hyperbaric oxygen.

Besides glucose, glutamine is also a major fuel for tumor cells.  Drugs will be required to target glutamine, as glutamine is the most abundant amino acid in the body and can be easily synthesized from glutamate.  Hyperbaric oxygen requires a patient to be enclosed in a pressurized oxygen chamber or room filled with pure oxygen at 2.5 x atmospheric pressure.

There is one highly encouraging case report for the success of this triple combination—hyperbaric oxygen, glucose inhibitors, and low-dose chemo—in which a late-stage, resistant breast cancer is driven to total remission.

Last week, a research paper from Duke U suggested a target for attacking the fermentation metabolism of cancer cells, and a marker for identifying which cancers are likely to be sensitive to it.

The research group of Jason Locasale found a protein called GAPDH which switches to the fermentation metabolism, and a compounded called koninjic acid, extracted from fungi, that inhibits GAPDH.  They have tested koninjic acid extensively in cell lines, and have begun testing in live mice.  Whether such drugs are more effective than simply restricting glucose is a topic for investigation.

Explanatory diagram from the Duke study of GAPDH

 

Mito-targeted Cancer Prevention

 Supplements that promote mitochondrial health include NMN, NR, CoQ10, PQQ, mitoQ/SkQ, alpha lipoic acid (ALA), carnitine, and melatonin.  Can they lower risk of cancer?  So far, we have just a few hints; this is a promising area for research.

CoQ10 was studied in the 1990s as a cancer treatment, with some encouraging results [ref].  PQQ has been shown to kill cancer in vitro [ref].

One mouse experiment looked at ALA as part of a cancer treatment [ref].  Use of carnitine remains theoretical [ref].  Most has been written about melatonin [ref, ref, ref], but even here, there is no epidemiological evidence.

 

The Bottom Line

All the evidence for radiation and other mutagens causing cancer might be re-interpreted in terms of mutations to mitochondrial DNA.  (Mitochondria live in the cytoplasm, outside the cell nucleus, but they have a bit of their own DNA and ribosomes for transcribing it.)

Damaged mitochondria can also cause cancer even when their DNA is intact, and Seyfried (after Warburg) makes a strong case that mitochondrial damage is the root cause of cancer.  Inflammation is probably the single worst source of mitochondrial damage. Do we need one more reason to minimize inflammation?

Viruses often target mitochondria for their own ends, and this may explain cases in which viral infections are associated with etiology of cancer.

The insight that mitochondrial damage is the root cause of cancer (preceding nuclear mutations) also has broad implications for cancer prevention.

As for treatment, there have been a few disappointments and also some promising pilot studies, especially in combining glucose deprivation with radiation or chemo to finish the job (“press-pulse”).  This is a research field that deserves much more attention.

Best Anti-aging supplements other than NR and NMN

22 Best Anti-Aging Supplements

Geroprotectors are substances that support healthy aging, slow aging, or extend healthy life. Sometimes people refer to them as “aging suppressants,” “anti-aging drugs,” “gerosuppressants,” “longevity therapeutics,” “senolytics,” or “senotherapeutics.” They include various foods, nutraceuticals (supplements), and pharmaceuticals (drugs). Unfortunately none comes close to realizing the age-old aspiration of ending aging altogether (yet), but some may make a practical difference for many people.

I’ve used several geroprotectors for years. And I’m exploring ways to incorporate others into my diet, if they’re applicable to my personal situation and meet a few general criteria:

First, I look for geroprotectors supported by multiple studies on humans – not just anecdotal evidence, one study, or studies on non-human animals. Although I’ve nothing against the health benefits of placebo, I prefer knowing that something more than only placebo is at work.

Second, I look for geroprotectors with the highest ratios of efficacy to expense. Given innumerable options and a limited budget, I want to do more than just empty my wallet.

Third, I look for geroprotectors that are legal and generally safe. If it’ll put me in a hospital or a prison, it’s not worth it.

Based on those criteria, I’ve compiled a list of top tier natural geroprotectors. These are, to the best of my knowledge, the most well-researched and effective geroprotectors available in the United States without a prescription. I’ve excluded from this list any geroprotectors that are primarily nootropic geroprotectors (such as ginkgo and melatonin), which you can find in my list of top tier nootropics. This information is for educational purposes only. It is not medical advice. Please consult a physician before and during use of these and other geroprotectors.

1) Berberine

Barberry

Berberine is a compound of extracts from herbs such as barberry. Supplementation may provide a strong decrease to blood glucose, and a notable decrease to total cholesterol, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Berberine may also provide a subtle increase to HDL-C; and a subtle decrease to insulin, LDL-C, and triglycerides. Evidence for these effects may not be as reliable. See the Berberine article  for more studies and details.

2) Blueberry

Blueberry

Blueberry is the fruit of a perennial flowering plant native to North America. Supplementation may provide a notable decrease to DNA damage, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

See the Blueberry article at Examine.com for more studies and details.

3) Boswellia Serrata (Frankincense)

Frankincense

Boswellia Serrata is a plant native to India and Pakistan. Supplementation may provide notable support for long-term joint function, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

See the Boswellia Serrata article at Examine.com for more studies and details.

4) Cocoa

Cocoa

Cocoa comes from the seeds of evergreen trees native to tropical regions of Central and South America. Supplementation may provide a notable increase to blood flow, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Cocoa may also provide a subtle increase to insulin sensitivity, and photoprotection; and a subtle decrease to general oxidation, platelet aggregation, and LDL-C. Evidence for these effects may not be as reliable.

5) Coenzyme Q10

Coenzyme Q10

Coenzyme Q10 is a molecule found in the mitochondria of humans and other organisms. Supplementation may provide a notable decrease to lipid peroxidation, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Coenzyme Q10 may also provide a subtle increase to blood flow, endothelial function, and exercise capacity; and a subtle decrease to blood pressure, exercise-induced oxidation, and general oxidation. Evidence for these effects may not be as reliable. See the Coenzyme Q10 article at Examine.com for more studies and details.

6) Creatine

Creatine

Creatine is a nitrogenous organic acid that occurs naturally in vertebrates. Supplementation may provide a strong increase to power output and a notable increase to hydration, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Creatine may also provide a subtle increase to anaerobic running capacity, lean mass, bone mineral density, muscular endurance, testosterone, VO2 max, and glycogen resynthesis; and a subtle decrease to blood glucose, lipid peroxidation, and muscle damage. Evidence for these effects may not be as reliable. See the Creatine article at Examine.com for more studies and details.

7) Curcumin

Turmeric

Curcumin is the bioactive in Turmeric, which is a perennial plant native to Southern Asia. Supplementation may provide a notable increase to antioxidant enzyme profile and a notable decrease to inflammation and pain, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Curcumin may also provide a subtle increase to HDL-C, and functionality in the elderly or injured; a subtle decrease to blood pressure, general oxidation, lipid peroxidation, and triglycerides; and subtle support for long-term joint function. Evidence for these effects may not be as reliable. See the Curcumin article for more studies and details.

8) DHEA (Dehydroepiandrosterone)

DHEA

DHEA is a natural hormone in humans and other animals. Supplementation may provide a notable increase to estrogen or testosterone (depending on the need of the body), according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

See the Dehydroepiandrosterone article at Examine.com for more studies and details.

9) Fish Oil

Fish

Fish Oil, as the name suggests, is an oil that accumulates in the tissues of some fish species. Supplementation may provide a strong decrease to triglycerides, thereby supporting a healthy cardiovascular system, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Fish Oil may also provide a subtle increase HDL-C, endothelial function, and photoprotection; and a subtle decrease to blood pressure, inflammation, natural killer cell activity, platelet aggregation, and LDL-C. Evidence for these effects may not be as reliable. See the Fish Oil article at Examine.com for more studies and details.

10) Garlic

Garlic

Garlic is a bulbous plant native to Central Asia. Supplementation may provide a notable increase to HDL-C and a notable decrease to LDL-C, total cholesterol, and blood pressure, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Garlic may also provide a subtle decrease to triglycerides and a strong decrease to rate of sickness. Evidence for these effects may not be as reliable. See the Garlic article at Examine.com for more studies and details.

11) Horse Chestnut (Aesculus Hippocastanum)

Horse Chestnut

Horse Chestnut is a deciduous flowering tree native to South East Europe. Supplementation may provide notable support to long-term circulatory function, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Horse Chestnut may also provide a subtle decrease to pain. Evidence for this effect may not be as reliable. See the Horse Chestnut article at Examine.com for more studies and details.

12) Magnesium

Magnesium

Magnesium is an essential dietary mineral found in food like nuts, cereals, and vegetables. Supplementation may provide a notable decrease to blood pressure (only in cases of high blood pressure), according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Magnesium may also provide a subtle increase to insulin sensitivity, aerobic exercise, and muscle oxygenation; and a subtle decrease to blood glucose, and insulin. Evidence for these effects may not be as reliable. See the Magnesium article at Examine.com for more studies and details. also check out my article on Magnesium Glycinate supplementation. Magnesium is an ingredient in Thrivous Serenity.

13) Nitrate

Beetroot

Nitrate is a molecule produced in the body in small amounts and available in vegetables like beetroot. Supplementation may provide a notable decrease to blood pressure, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Nitrate may also provide a notable increase to anaerobic running capacity; and a notable decrease to oxygenation cost of exercise. Evidence for these effects may not be as reliable.

14) Olive Leaf

Olive Leaf

Olive Leaf comes from an evergreen tree native to the Mediterranean, Africa, and Asia. Supplementation may provide a notable decrease to blood pressure and oxidation of LDL, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Olive Leaf may also provide a subtle increase to HDL-C; and a subtle decrease to LDL-C, total cholesterol, cell adhesion factors, and DNA damage. Evidence for these effects may not be as reliable. See the Olive Leaf Extract article at Examine.com for more studies and details.

15) Pycnogenol (Pine Bark)

Maritime Pine

Pycnogenol is an extract from bark of the maritime pine, native to the Mediterranean. Supplementation may provide a notable increase to blood flow, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Pycnogenol may also provide a subtle decrease to leg swelling; and subtle support for long-term joint function. Evidence for these effects may not be as reliable. See the Pycnogenol article at Examine.com for more studies and details.

16) Salacia Reticulata

Salacia Reticulata

[“Kothala Himbutu” by Satheesan.vn under CC BY-SA 3.0 / cropped]

Salacia Reticulata is a plant native to the forests of Sri Lanka. Supplementation may provide a notable decrease to blood glucose and insulin, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

See the Salacia Reticulata article at Examine.com for more studies and details.

17) SAMe (S-Adenosyl Methionine)

SAMe

SAMe is a naturally-occurring compound found in most tissues and fluids of the human body. Supplementation may provide notable support for long-term joint function, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with SAMe may also provide a subtle increase to functionality in elderly or injured; and a notable decrease to pain. Evidence for these effects may not be as reliable. See the S-Adenosyl Methionine article at Examine.com for more studies and details.

18) Spirulina

Spirulina

[“Spirulina” by Lara Torvi under CC BY 2.0 / cropped]

Spirulina is a blue-green algae. Supplementation may provide a notable decrease to lipid peroxidation and triglycerides, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Spirulina may also provide a strong decrease to allergies, nasal congestion, and liver fat; a notable increase to power output; a notable decrease to blood pressure and general oxidation; a subtle increase to HDL-C and muscular endurance; and a subtle decrease to LDL-C and total cholesterol. Evidence for these effects may not be as reliable. See the Spirulina article at Examine.com for more studies and details.

19) TUDCA (Tauroursodeoxycholic Acid)

TUDCA

TUDCA is a bile acid found naturally in trace amounts in humans and in large amounts in other animals like bears. Supplementation may provide a notable decrease to liver enzymes, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with TUDCA may also provide a notable increase to insulin sensitivity. Evidence for this effect may not be as reliable. See the Tauroursodeoxycholic Acid article at Examine.com for more studies and details.

20) Vitamin B3 (Niacin)

Niacin

Vitamin B3, also known as Niacin, is an essential dietary vitamin found in foods like liver, chicken, beef, fish, peanuts, cereals, and legumes. Supplementation may provide a strong increase to HDL-C and a notable decrease to LDL-C and triglycerides, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Vitamin B3 may also provide a subtle increase to blood glucose and insulin; and a subtle decrease to insulin sensitivity and vLDL-C. Evidence for some of these effects may not be as reliable. See the Vitamin B3 article at Examine.com for more studies and details.

21) Vitamin D

Vitamin D3

Vitamin D is an essential dietary vitamin naturally synthesized in the skin from sun exposure. Supplementation may provide a notable decrease to risk of falls, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Vitamin D may also provide a notable increase to functionality in elderly or injured; and a subtle decrease to blood pressure, bone fracture risk, and fat mass. Evidence for some of these effects may not be as reliable. See the Vitamin D article at Examine.com for more studies and details.

22) Vitamin K

Vitamin K1

Vitamin K is an essential dietary vitamin found in foods like leafy green vegetables and some fruits. Supplementation may provide a notable increase to bone mineral density, according to multiple peer-reviewed, double-blind, placebo-controlled studies in humans:

Supplementation with Vitamin K may also provide a notable decrease to bone fracture risk. Evidence for this effect may not be as reliable. See the Vitamin K article at Examine.com for more studies and details.

Fasting decreases hunger which makes it more effective than dieting

Ghrelin is the so-called hunger hormone, first purified from rat stomach in 1999 and subsequently cloned. It binds to growth hormone (GH) secretagogue receptor, which strongly stimulates GH. So, eating, by itself does not makes you gain lean tissue (like muscle and bone), despite what all the makers of supplements like whey protein and creatine claim. Rather, hunger may be a strong growth stimulus.

Nothing turns off Growth Hormone like eating and you need GH to grow functional tissue. Of course, food provides the nutrients needed to grow, so in fact, you need both feeding and fasting cycles to properly grow. Not all feeding, and not all fasting. Life lies in the balance of the two. The cycle of life is feast and fast. But in today’s world, many people would have you believe that fasting is detrimental to your health, and that you should eat all the time.

The biggest worry about fasting is dealing with hunger. People assume that hunger will get worse and worse until you cannot help yourself and start an IV donut slurry in your garage. Oooh… donuts…. Ghrelin, the hunger hormone, increases appetite and weight gain. It also antagonizes the effect of leptin (in rats at least). Leptin is a hormone produced by fat cells which turns off appetite and makes us stop eating.

Ghrelin turns on appetite. So, if you want to lose weight on a long term basis, you need to tune down ghrelin. If you don’t eat (fast), don’t you get hungrier and hungrier, ghrelin goes up and up and you’ll just gain weight?

Well, no. As we discussed last week, eating all the time sounds like it will turn off hunger and ghrelin. But that’s far too simplistic. Surprisingly, the answer to turning down ghrelin (and hunger) is the opposite — fasting.

Let’s look at this study “Spontaneous 24-h ghrelin secretion pattern in fasting subjects“. Patients undertook a 33 hour fast, and ghrelin was measured every 20 minutes. Here’s what ghrelin levels look like over time.

There are several things to notice. First, ghrelin levels are lowest at approximately 8:00 – 9:00 in the morning.

Circadian rhythm studies consistently find that hunger is lowest first thing in the morning, also generally the longest period of the day where you have not eaten.

This reinforces the fact that hunger is not simply a function of ‘not having eaten in a while’. At 9:00, you have not eaten for about 14 hours, yet you are the least hungry. Eating, remember, does not necessarily make you less hungry.

Next, notice that there are 3 distinct peaks corresponding to lunch, dinner and the next day’s breakfast. BUT IT DOES NOT CONTINUALLY INCREASE. After the initial wave of hunger, it recedes, even if you don’t eat.

Ghrelin shows a “spontaneous decrease after approximately 2 h without food consumption”. This correlates perfectly to our clinical experience in the Intensive Dietary Management Program that ‘hunger comes in waves’.

If you simply ignore it, it will disappear. Think of a time that you were too busy and worked right through lunch. At about 1:00 you were hungry, but if you just drank some tea, by 3:00 pm, you were no longer hungry. I often feel the same level of hunger whether I ate lunch or not — exactly what the ghrelin studies show. Ride the waves — it passes.

Also note that ghrelin does have a learned component since all these subjects were used to eating 3 meals per day. It is not merely by coincidence that these peaks of ghrelin happen. This is similar to the ‘cephalic phase’ of insulin secretion that we’ve discussed previously.

There was one other big finding of this study. Look at the average ghrelin levels over 24 hours. Over the entire day of fasting, ghrelin stays stable! In other words, eating nothing over 33 hours made you no more or less hungry than when you started! Whether you ate or did not eat, your hunger level stayed the same.

Eating more sometimes makes you more hungry, not less. In the same vein, eating less can actually make you less hungry. That’s terrific, because if you are less hungry, you will eat less, and are more likely to lose weight.

So what happens over multiple days of fasting? This study looked at the question specifically. 33 subjects had their ghrelin measured over 84 hours of fasting and they divided the results by men and women, as well as obese and lean.

There were no significant differences between the lean and obese subjects, so I won’t dwell on that further. Once again, there were distinct circadian variations.

Over 3 days of fasting, ghrelin gradually DECREASED. This means that patients were far LESS hungry despite not having eaten for the past 3 days. This jives perfectly with our clinical experience with hundreds of patients undergoing extended fasting in our IDM program.

Everybody expects to be ravenously hungry after fasting multiple days, but actually find that their hunger completely disappears.

They always come in saying ‘I can’t eat much anymore. I get full so fast. I think my stomach shrank’. That’s PERFECT, because if you are eating less but getting more full, you are going to be more likely to keep the weight off.

 

Notice, also the difference between men and women. There’s only a mild effect for men. But the women show a huge decrease in ghrelin. Again, this addresses one of the major worries that women are not able to fast.

Actually, women would be expected to have more benefit from fasting because their hunger can be expected to decrease better than men. Notice, too, how much higher women’s ghrelin level reaches.

I suspect this correlates to the clinical observation that many more women are ‘addicted’ to certain foods eg. chocoholics. Sugar addicts. etc.

So many women have remarked how a longer fast seemed to completely turn off those cravings. This is the physiologic reason why.

A few other notes about the hormonal changes of fasting. Notice that cortisol does go up during fasting.

Yes, fasting is a stress to the body and cortisol acts as general activator as well as trying to move glucose out of storage and into the blood. So, if too much cortisol is your problem, then fasting may not be right for you.

Insulin also goes down, which is what we expect. Growth hormone, as we’ve previously noted, goes up during fasting. This helps to maintain lean muscle tissue and to rebuild lost protein when you start to eat again.

An interesting study of food cravings found exactly what we have been discussing. When patients were put on low calorie diet (1200) versus very low calorie (500) diets, food cravings didn’t change much on the former, but virtually disappeared on the latter. Yes. By eating almost nothing, food cravings did not get worse, they got much, much better.
This effect on food cravings is true for all food, since all foods are restricted. So cravings for sweets, carbs and high fat foods are all reduced.
This is very important in the fight to lose weight. Controlling hunger by eating little bits at a time simply does not work.

During intermittent and extended fasting, ghrelin, the main hormonal mediator of hunger does not increase to unmanageable levels. Rather it decreases — which is exactly what we are looking for.

We want to eat less, but be more full. Fasting, unlike caloric restriction diets is the way to do that.

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.

Mitochondria in Aging, II: Remedies

The once-popular mitochondrial free radical theory of aging proved to be too glib. Aging isn’t fundamentally about dispersed damage; rather, dispersed damage is a result when the body’s defenses stand down in old age.  Nevertheless, the mitochondria do play a role in aging, largely through signaling and apoptosis.  Antioxidants targeted to mitochondria may be an exception to the rule that antioxidants don’t prolong lifespan.  And other supplements and strategies that either promote production of new mitochondria or enhance their efficiency of operation show promise for modest lifespan extension.


Growing new mitochondria

A ketogenic diet leads to generation of new mitochondria, as do caloric restriction and exercise.  Exercise when the body is starved for sugar (low glycogen) is the most potent stimulator of new mitochondrial growth.  Exercise while fasting, or continue to exercise after you “hit your wall”.

Hormones that promote mitochondrial proliferation include thyroxin, estrogens, and glucocorticoids.  Promoting new mitochondria has a tendency simultaneously to suppress apoptosis, programmed cell death [ref].  At later ages, apoptosis of cells that are still functional tends to be a larger problem than the failure of cancerous cells to eliminate themselves by apoptosis.  In other words, suppressing apoptosis is (on balance) a good thing for anti-aging, but the downside is it can also increase risk of cancer.

 

Ubiquinone=CoQ10

Coenzyme Q-10 (aka ubiquinone) is an essential part of mitochondrial chemistry, shuttling electrons along their way to the ATP molecules that mitochondria generate as their primary energy export to the cell.  It’s often called an antioxidant, but that’s not the primary role of CoQ10.

As a supplement, it is well-established with a good reputation.  There is lots of evidence for benefits to health markers, especially athletic endurance, several aspects of heart health, and erectile dysfunction.  If you have fibromyalgia or if you are taking statins, CoQ10 is strongly indicated.  For chronic fatigue syndrome, it’s definitely worth trying.

But there’s no reason to expect it will increase your life expectancy.  Supplementing with ubiquinone increases the lifespan of worms but not mice or rats [ref, ref].

Worms that cannot make unbiquinone live 10 times as long.  Just saying…

A few years ago, ubiquinol was introduced as a more bioavailable form of ubiquinone.  It’s more expensive, but there is not clear evidence that it is more bioavailable.

 

PQQ

Pyrroloquinoline quinone is helpful but not necessary part of mitochondrial chemistry.  Bacteria make a lot of it; plants less; mammals only tiny quantities.  Mice completely deprived of PQQ show growth deficiency, but the amount that they need is tiny compared to the quantities in PQQ supplements.

PQQ is a growth factor for bacteria, and the principal health claim for PQQ is that it can stimulate growth of new mitochondria.  The evidence is based on biochemistry and cell cultures.  In live mice, it has been shown that PQQ deficiency results in a mitochondria deficiency, but not that large quantities of PQQ lead to more mitochondria.

Bill Faloon (LEF) and Joseph Cohen (selfhacked) are big fans of PQQ, and you can read a list of benefits here.  Cohen claims PQQ helps with sleep quality and nerve growth, leading to better cognitive function.

Small quantities of PQQ can be absorbed from many plant foods, but not animal foods.  Much larger quantities come in supplement form. 100 g of tofu has just 2µg (micrograms).  Supplements are usually 5-20 mg, hundreds of times as much as you’re likely to get from a vegetarian diet.  Here is a table of PQQ concentrations in foods:

 

SkQ and MitoQ

These are two closely related molecules, originally synthesized in Russia in the 1970s, but it wasn’t until the 1990s that their therapeutic value was documented by two New Zealand scientists.  One end of the molecule is CoQ10 (or a version found in plants, claimed to be even more powerful as an antioxidant).  The other end of the molecule is an electric tugboat that pulls the molecule into mitochondria.

I’ve written a  detailed report three years ago.  At the time, I noted that the Russians claimed to extend lifespan of mice modestly with SkQ, and SkQ was found (also in Russian labs) to be a powerful rejuvenant for aging eyes.  The Russians sell SkQ as eye drops.  The Kiwis sell MitoQ as skin cream and also as pills.

Earlier this year, the Russian labs announced that SkQ had substantially extended lifespan of a mouse strain that was short-lived because of a mitochondrial defect.  None of the Russian claims have been reproduced in Western labs.  Three years ago, I was inclined to give the Russians the benefit of the doubt, but now I’m starting to wonder, since the New Zealand company has a laboratory arm, and they haven’t announced anything nearly so impressive.

 

Humanin and her sisters

Mitochondria have ringlets of their own DNA, encoding just 37 genes.  (That doesn’t mean that the mitochondria only need 37 proteins; the great majority of proteins needed by mitochondria are coded in chromosomes of the cell nucleus, and transported to the mitochondria as needed.)  Just 16 years ago, the first mitochondrial-coded protein to be discovered was named Humanin, because it was found to improve cognitive function to dementia patients, restoring some of their “humanity”.  In addition to being neuroprotective, humanin promotes insulin sensitivity.  Humannin’s action is not confined to the mitochondrion in which it was produced, but in fact it  circulates in the blood as a signal molecule.  Blood levels of humanin decline with age.

Humanin

In experiments with mice, humanin injections have been shown to protect against disease.  Lifespan assays with humanin are not yet available.

To date, HN and its analogs have been demonstrated to play a role in multiple diseases including type 2 diabetes (25, 43), cardiovascular disease (CVD) (2, 3, 47), memory loss (48), amyotrophic lateral sclerosis (ALS) (49), stroke (50), and inflammation (22, 51). The mechanisms that are common to many of these age-related diseases are oxidative stress (52) and mitochondrial dysfunction (53). Mitochondria are major source of ROS, excess of which can cause oxidative damage of cellular lipids, proteins, and DNA. The accumulation of oxidative damage will result in decline of mitochondrial function, which in turn leads to enhanced ROS production (53). This vicious cycle can play a role in cellular damage, apoptosis, and cellular senescence – contributing to aging and age-related diseases. Indeed, oxidative stress is tightly linked to multiple human diseases such as Parkinson’s disease (PD) (54), AD (55), atherosclerosis (56), heart failure (57), myocardial infarction (58), chronic inflammation (59), kidney disease (60), stroke (61), cancers (62, 63), and many types of metabolic disorders (64, 65). We and others have shown that HN plays critical roles in reducing oxidative stress (6668). [2014 review]

Pinchas Cohen, MD (Dean, School of Gerontology, University of Southern California Davis, Los Angeles, California) is an expert in humanin, a protein (peptide) produced in mitochondria. Mitochondria are energy-generating organelles in cells, which have their own DNA separate from the DNA in the nucleus. The amount of DNA found in the mitochondria is much less than that found in the nucleus. As such, mitochondrial DNA contains codes for only a few proteins, humanin being one of them. Humanin was discovered by a search for factors helping to keep neurons alive in undiseased portions of the brains of Alzheimer’s disease patients.Humanin protects neurons against cell death in Alzheimer’s disease, as well as protecting against toxic chemicals and prions (toxic proteins)[ref].  Dr. Cohen’s team has shown that humanin also protects cells lining blood vessel walls, preventing atherosclerosis. In particular, they have shown that low levels of humanin in the bloodstream are associated with endothelial dysfunction of the coronary arteries (arteries of the heart).[ref] Humanin has also been shown to promote insulin sensitivity, the responsiveness of tissues to insulin. Because humanin levels decline with age, it is believed that reduced humanin contributes to the development of aging-associated diseases, including Alzheimer’s disease and type II diabetes. [Ben Best]

Personal notes: This lab near where I am visiting in Beijing is taking leadership in characterizing a group of short peptides similar in origin to humanin, and this company across the street from us is selling mitochondrial peptides.

If humanin were a patentable drug, there would be much excitement and multiple clinical trials for AD, probably leading to expansion into general anti-aging effects.

 

MOTS-c

This is another short peptide of mitochondrial origin, only recently discovered and characterized.  I was alerted to its existence by a study from a USC lab that was written up here in ScienceBlog just this month (reprinted from a USC press release).  Results are new but impressive.  Mice injected with MOTS-c had more muscle mass, less fat, more strength and endurance.  MOTS-c protected their insulin sensitivity when mice were fed a high fat diet [ref].  Lifespan studies haven’t been done yet.

Like humanin, MOTS-c is manufactured inside mitochondria from a template in mitochondrial DNA, but it is exported from the cell and appears in the bloodstream as a signal molecule.  Blood levels of MOTS-c decline with age.  It is a mini protein molecule with 16 amino acids, too big to survive digestion so it can’t be taken orally.

“MOTS-c holds much potential as a target to treat metabolic syndromes by regulating muscle and fat physiology, and perhaps even extend our healthy lifespan.”[ref]

Let’s keep your eyes on this one over the next year or two.

 

Gutathione / NAC

I’ve never heard anyone say a bad word about glutathione.  It’s the antioxidant with no downside.  Genetic modifications that upregulate glutathione have increased lifespan in worms, flies and mice.

For a long while, it has been assumed that you can’t eat glutathione, because it doesn’t survive digestion.  Some researchers at Penn State disagree, finding impressive increases in tissue and blood levels when people were supplemented with up to 1 g per day raw glutathione.  Liposomal glutathione is an oral delivery form that gets around the digestion problem, especially when taken with methyl donors like SAMe.

The herb Sylimarin=milk thistle may increase glutathione.  For now, the precursor molecule N-Acetyl Cysteine (NAC) is the best-established supplement we have to promote glutathione.  In the one available study, supplementing with NAC greatly increased lifespan in male but not female mice.  NAC also increases lifespan in worms and flies.

N-Acetyl Cysteine

Glutathione

 

For the future, we might hope to do better.  Less than 20% of the cell’s glutathione actually makes its way to the mitochondria, where it is most needed.  There are esters of glutathione that, in theory, ought to be attracted into the mitochondria.  They have been tested in cell culture only, but are more than ripe for animal testing [ref].

 

Nicotinamide Riboside (NR) and other NAD+ enhancers

The chemicals NAD+ and NADH are alternative, cycled forms of an intermediate in the process by which mitochondria make energy.  Levels of NAD+/NADH decline with age.  NR is a precursor to NAD+, and it has been demonstrated (preliminary results in humans) that NR supplementation increases blood levels of NAD+.

It may be awhile before we know for sure whether this leads to better health or longer lifespan.  Niagen and Basis are heavily promoted with credible scientifists behind their products, and many early adopters offer subjective reports of short-term benefits.  There is one mouse study claiming to pull a 3% extension of lifespan out of the noise, and perhaps I am less open to the finding because the article, published prominently in Science, seems so breathless in describing benefits.

 

Melatonin

The primary role of melatonin is to regulate the body’s sleep/wake cycle.  Melatonin declines with age and the timing of our daily melatonin surge gets fuzzier and less reliable with age.sleep quality deteriorates.  Sleep quality suffers.

Melatonin is well-established in mice as a modest longevity aid, although results have been inconsistent.  12 out of 20 studies showed a lifespan increase, and the remaining 8 showed no increase or decrease.  Whether nightly supplementation affects mortality rates in humans has never been determined.

Melatonin is concentrated in mitochondria as much as 100-fold, and it may even be created there [ref], independent of the circulating melatonin that is secreted from the pineal gland at night.  One of its actions is as a mitochondrial antioxidant and scavenger of ROS.

Twenty years ago, Walter Pierpaoli promoted melatonin as a sleep aid, cancer fighting hormone that would enhance your mood and your sex life while keeping you young.  Russian labs have also been optimistic.  My take is that melatonin is a legitimate anti-aging hormone, and is especially useful for those of us whose sleep is disrupted with age.  It is widely available, cheap and safe.  Unless you’re fighting jet lag, 1 to 2 mg at night is all you need.

Also worth mentioning

Magnesium is required for manufacture of glutathione.  Selenium works along with glutathione.  Omega-3 fatty acids can promote synthesis of glutathione.  Acetyl L-carnitine transports fat fuels through the mitochondrial membrane.  Alpha-lipoic acid is part of the mitochondrial energy metabolism.

The Bottom Line

Commercial interests can make some messages louder than others, and the health news we hear is affected by what is profitable as much as by what is healthy.  Exercise is primary, but has no sales value.  Of the supplements reviewed here, NAC is the best-established for mitochondrial health and a possible effect on lifespan.  It is cheap and available.  Liposomal glutathione is certainly more expensive and possibly more effective.  Melatonin is even cheaper, and has been found to increase lifespan in multiple rodent studies, with broad benefits apart from modification of mitochondrial function.  Humanin and MOTS-c, not yet close to commercial availability, seem to be promising substances to explore for health, though not for profits.

Mitochondria in Aging, I Mechanisms and Background

A popular theory a generation back sought to trace aging to oxidative damage originating in the mitochondria.  Every cell in the body has hundreds or thousands of mitochondria, the sites of the high-energy chemistry that produces ROS as toxic waste. The hope was that by quenching the ROS, aging might be turned off. The “Mitochondrial Free Radical Theory” is built on a flawed theoretical foundation, and anti-oxidants don’t extend lifespan. Nevertheless, the mitochondria play a role in aging.  Historically, mitochondria were mediators of the first organized mechanisms of programmed death over a billion years ago, and they retain a role in processing signals that regulate lifespan.  Curiously, though a quadrillion mitochondria are dispersed through the body, they act in some ways like a single organ, sending coordinated signals that regulate metabolism and affect aging.


Mitochondria are in the cells of all plants and animals—hundreds or thousands of mini power plants in each cell.  They burn sugar to make electrochemical energy in a form the cell can use.  They are loyal and essential servants.  But it wasn’t always so.  More than a billion years ago, mitochondria came into the cell as invading bacteria.  Though they’ve long ago been domesticaed, they retain a bit of their autonomy as a relic of the past.  Mitochondria have their own DNA.  Like bacteria, mitochondrial DNA is in the form of loop, a plasmid rather than a chromosome.  Each mitochondrion keeps several copies of the plasmid.

Mitochondria retain from their distant pathological past the capacity to kill the cell.  This is an orderly process known as apoptosis=programmed cell death.  Mitochondria are not the jurors that sentence the cell to death, but only the executioners acting on external signals.

Aging of the body as a whole is centrally coordinated, though the nature and location of the clock(s) remain a major unsolved problem.  Communication about the age state of the body is carried through signal molecules in the blood, and tissues respond accordingly.  Mitochondria not only pick up on these signals, they also contribute circulating signals of their own.  Apoptosis is dialed up in old age.  Along with inflammation, it is a primary, local mode of the self-destructive process that is aging.  We lose too many cells to apoptosis, cells that are still healthy and useful, and mitochondria are the proximate cause of this loss.

Portrait by scanning electron microscope, artistically colorized

 

Signaling, up, down and sideways

The big picture is that mitochondria take their orders from the cell nucleus, where the vast majority of the DNA is housed.  The transcription factors that determine what mitochondrial genes are expressed are housed in the nucleus.  In addition, there is feedback, retrograde signaling, by which mitochondria communicate to the nucleus the state of their own health and of the cell’s energy mtabolism in general.  The nucleus responds with changes in transcription based on communication from the mitochondria.

A great part of the diverse benefits of caloric restriction, and perhaps of exercise, too, are thought to originate in signaling from the mitochondria.

In addition to sending and receiving signals from the cell nucleus, mitochondria talk to each other.  They coordinate extensively within a cell, and they also generate hormones that are transmitted through the bloodstream, talking to distant cells and foreign mitochondria.

 

Mitochondria and Cancer

Cancer cells have impaired mitochondrial metabolism.  They don’t burn sugar through the usual, high-efficiency mode that combines with the maximal amount of oxygen; rather they use fermentation—anaerobic breakdown of sugar.  Cancer cells do this even when oxygen is plentiful, despite the fact that it generates much less energy per sugar molecule.  Cancer cells are starved for energy, and they gobble up sugar at a high rate.  (PET scans are able to visualize tumors on the basis of their sugar consumption.)  Eating a very-low-carb diet is a cancer therapy.

90 years ago, a Nobelist and Big Thinker in biomedicine named Otto Warburg gave us the hypothsis that mitochondria with impaired glucose metabolism are the root cause of cancer.  We usually think of cancer as starting with mutations that lead to uncontrolled growth and proliferation, but in the Metabolic Theory of Cancer, mutations and proliferation are secondary to this change in mitochondrial chemistry.  Today, proponents of the Warburg Hypothesis are a small but enthusiastic minority, armed with facts and arguments that I have not yet found time to assess.  But I am struck by the fact that when the nucleus of a cancer cell is transplanted into a healthy cell, the healthy cell remains healthy; and when the nucleus of a healthy cell is transplanted into a cancer cell, the cell remains cancerous [ref, ref].  This seems to be prima facieevidence that the essence of cancer is not to be found in chromosomes of the nucleus.

 

Fewer, less efficient, and more toxic waste with age

We have fewer mitochondria as we age, and this is plausibly connected to lower muscle strength and endurance as well as energy in the organ that uses energy most intensively=the brain [ref].  The relationship is subtle enough that it is not completely nailed down, despite decades of work from true believers.  Since mitochondria mediate apoptosis, it is also plausible that loss of muscle cells and nerve cells with age (at least partially through apoptosis) is also mediated by mitochondria.

Cells that need a lot of energy have a lot of mitochondria. Heart muscle cells are packed with them.

Compounding the problem, the mitochondria that we do have become less efficient with age.  They are giving us less energy, and they are generating more reactive oxygen species (ROS).  Simultaneously, the cell is generating less of the native anti-oxidants that protect from ROS.  Glutathione, ubiquinone, and superoxide dismutase all decline with age.  This is one of the ways the body destroys itself.  Oxidative damage accumulates in old but not young people.  Oxidative damage may also contribute to telomere shortening.

Somehow, ROS generated by impaired mitochondria produce damage that accumulates, but ROS generated by exercise signal the body to ramp up the repair processes, and produce a net gain in health.  It is not clear how the two processes are distinguished.  The reason that anti-oxidants don’t work to extend lifespan is probably that they interfere with the signaling functions of ROS.

The best-documented way in which mitochondria deteriorate is that their DNA develops mutations.  I find this something of a conundrum—not that mitochondria should accumulate mutations over the course of a lifetime but that they don’t accumulate mutations from one generation to the next (in the germline).  Mitochondria proliferate clonally, without sex.  Sex shuffles genes in many combinations, so that the good genes can be separated from the mutated ones, and the latter eliminated before they get fixed into the genome.  Without sex, how do mitochondria avoid accumulating mutations over the aeons?  And since they largely do manage to avoid accumulating mutations over millions of years, why can’t they avoid accumulating mutations over the course of a few decades within a human body?

 

Are mutations in mitochondrial DNA a cause of aging?

Mitochondrial mutations accumulate with age.  Genetically modified mice with a defective gene for replication of mitochondrial (but not nuclear) DNA age faster and die earlier.  This has generally been taken as proof that mitochondrial mutations are a factor in aging, but it need not be so.  In fact, mitochondria function well with a high tolerance for genetic errors, and it is not clear whether levels of mitochondrial mutations in aging humans cause significant problems, or even whether mutations are related to the general decline in mitochondrial function with age.  An alternative explanation for the mito-mutator mice is that they have developmental problems already in utero, and these may lead to premature aging even without accumulation of mito mutations.

Mitochondrial mutator mice

Stem cells keep dividing and producing new functional (differentiated) cells through the life of the animal.  They seem smart enough to minimize the damage from mitochondrial mutations.  Stem cells have been observed to hold on to the best mitochondria, and pass the damaged ones off to the cells that have a limited lifetime. This helps keep the errors from proliferating, and is in the best interest of the organism as a whole.  It’s interesting that mother budding yeast cells do the opposite—they hold on to their damaged mitochondria and pass the cleanest and purest on to their daughter cells [ref].  Mammalian mothers also seem able to choose the best mitochondria to pass to their daughters, purifying the germline [ref].  In other words, though their behavior is the opposite of stem cells, both behaviors are adaptive for the long-term interest of the organism (and its progeny).

In summary, the age-related increases in oxidative damage and ROS production are relatively small and may not explain the rather severe physiological alterations occurring during aging. Consistent with this hypothesis, the absence of a clear correlation between oxidative stress and longevity [across species] also suggests that oxidative damage does not play an important role in age-related diseases (e.g., cardiovascular diseases, neurodegenerative diseases, diabetes mellitus) and aging. Experimental results from mtDNA mutator mice suggest that mtDNA mutations in somatic stem cells may drive progeroid phenotypes without increasing oxidative stress, thus indicating that mtDNA mutations that lead to a bioenergetic deficiency may drive the aging process [but this is not assured, since these mice seem to suffer substantial damage already in utero]. There is as yet no firm evidence that the overall low levels of mtDNA mutations found in mammals drive the normal aging process. One way to address this experimentally would be to generate anti-mutator animal models to determine whether decreased mtDNA mutation rates prolong their life span. [Bratic & Larsson review]

 

Mitochondrial evolutionary conundrum

Mitochondria reproduce clonally, like bacteria.  In fact, all the mitochondria in your body were inherited from one of your mother’s egg cells, and she got her mitochondria from your maternal grandmother, and so forth back in time—matrilineal all the way.  How is it that defects don’t accumulate in the mitochondrial genome?

As far as I know, the way in which the integrity of the mitochondrial genome is maintained remains an unsolved problem.  We do know that mutations in mitochondrial DNA increase with age in some tissues but not others [ref].  The reason you have to speak up when you talk to your grandmother is probably related to mitochondrial defects in neurons [ref].

Over the course of millions of years, mitochondria do not lose their genetic integrity, though the mitochondrial genome evolves more rapidly than the nuclear genome, and different species tend to have distinctive mitochondrial genomes.  The mystery is why detrimental mutations should accumulate over decades, but not over aeons.

To me, this is powerful evidence that there is a mechanism for managing the evolution of the mitochondrial genome.  It probably involves selection by the cell so that mitochondria that are functioning efficiently are encouraged to reproduce.  The cell acts like a human lab that is breeding tomatoes or Labrador retrievers for specific characteristics that the breeder or the cell finds most useful.  Probably there is also gene exchange among the different copies of the plasmid within a mitochondrion, and between mitochondria as they sometimes merge during the lifetime of a cell (my speculation).

 

What’s going on?

A theme in this blog (and in my thinking) has been that aging is not a dispersed process of locally-occurring damage, but is centrally orchestrated.  Well, mitochondria are about as far from “central” as you can get.  We have about a quadrillion of them, dispersed through every cell in the body (except red blood cells).

Mitochondria talk to each other within a single cell.  They merge and they reproduce, coordinating with one another and with the cell nucleus.  Now it appears they also send signals through the bloodstream (more next week).  Could they be acting like a single organ, dispersed through the body? Maybe.  Sensing the body’s state of energy usage and fuel sufficiency, they send signals that contribute to calculations about lifespan.

My guess is that aging is coordinated by a few biological clocks (centralized like the suprachiasmatic nucleus and the thymus or dispersed like telomeres and methylation patterns), and that mitochondria are not counted among the clocks.  But mitochondria are important intermediates.  The old story is that they generate energy and generate tissue-damaging ROS.  The new story is that they are also centers of signal transduction, probably based on their first-hand knowledge of the energy status of the body.

GMO Foods You Should Avoid Completely

Not everyone is familiar with GMO. People don’t know what it means and what its side effects are. Well, you’re in for a surprise. More than likely, we are taking in GMO food every single day. And we should be alarmed.

What Is GMO Food

GMO means “genetically modified organisms.” These are organisms that have changes introduced into their DNA via genetic engineering. Genetic engineering is the direct manipulation of an organism’s genome using biotechnology. It allows the introduction of new traits into an organism.

Scientists and biochemists combine genes from plants, animals, bacteria, and viral gene pools. This creates crossbreeds of unique crops.

History of GMO Food

Crops have been modified for thousands of years. Even in the prehistoric times, humans have already been tinkering with food and their genes. They strove to improve crops’ satisfaction to humans, durability, and resistance to disease and pests.

Over the years, humans have been molding crops into things that would never survive without the care of humans. Plants that we know now are a far cry from the plants they were back in the day. Back then, they were left untouched and unmodified.

During the 1970s, two US biochemists developed a technique that allowed DNA to be cut in certain places. These were then attached to the DNA of other organisms. Modern biotechnology is born. Later, biotechnology became commercialized. Companies started to experiment with inserting genes from one species to another.

In the present day, there is still much debate about GMO food. Though the FDA has listed them as safe, some are still wary with consuming GMO food. Some fear that eventually, there will be harmful consequences to humans.

Top GMO Food to Avoid

Corn

This may surprise you, but there are over 142 different types of genetically modified corn. This is the most of any plant species. Because of genetic modification, this corn creates its own insecticide. Monsanto, an American agrochemical and agricultural biotechnology corporation, has revealed that half of the United States’s sweet corn farms are using genetically modified seed.

Soy

Thanks to genetic modification, soy now resists herbicides. Its products include tofu, soy beverages, soy flour, and soybean oil. Other products include baked products and edible oil.

Genetically modified soy is in animal feed and in soybean oil. Many restaurant chains use soybean oil. Processed food contains this oil as well. It also produces soy lecithin. This emulsifier is present in many processed food, like dark chocolate bars and candy.

Cotton

The cotton plant resists pesticides as well. Cottonseed oil is from genetically modified cotton. This oil is for frying in fast-food restaurants and is also in packaged food. Potato chips, oily spreads (like butter and margarine), even cans of smoked oysters are some examples.

Some parts of the cotton plant are also used to create food fillers (such as cellulose). They are also in animal feed.

Hawaiian Papaya

The papayas that we munch on, we get them from the beautiful island of Hawaii. Genetically  modified papaya was introduced to the papaya plantations there in 1999. This type of papayas can withstand the ringspot virus.

At present, this GMO food covers about one thousand hectares of land.

Zucchini and Yellow Squash

These vegetables resist pathogens and certain types of fungi. In the United States, six varieties of this virus-resistant GMO food is sold. However, the number of these genetically modified vegetables are quite small as compared to other GMO food available in the country.

Sugar Beets

This is a very controversial vegetable. First, they gained approval in 2005. Then in 2010, USDA banned sugar beets. Finally, in 2012, the USDA officially deregulated them.

More than half of the granulated sugar production in the United States come from genetically modified sugar beets. Because of engineering, these beets resist glyphosates (weed killers).

Canola Oil

Genetically modified canola oil basically produces cooking oil. Margarine also comes from this GMO food. In addition, it also produces emulsifiers. Emulsifiers are food additives that stabilize food products. Processed food have emulsifiers.

Its genetically modified form gained approval in 1996. And as of 2006, it was estimated that around 90 percent of Canada’s and the United States’s canola crops are genetically modified.

Milk

In the United States milk industry, it’s quantity over quality. Cows receive rBGH (recombinant bovine growth hormone). This forces the cows to increase the amount of milk produced by 15 percent. Poor cows.

The milk from these engineered cows contains increased levels of IGF-1 (insulin growth factors-1). Studies show there is a connection between high levels of IGF-1 in humans and breast cancer and colon cancer.

Take note that many countries ban the use of rBGH. These include Canada, New Zealand, Australia, Japan, and the European Union.

Corn Starch

Corn starch has a number of uses. First, in cooking, it is a thickener for sauces, yogurt, and gravy. In baked goods, it gives structure to the pastries and adds fullness and moisture to them. Finally, in fried food, it provides a light and crispy texture to the batter.

But corn starch is one of the unhealthy ingredients we should avoid.

To start, corn starch is from a GMO food—corn. Corn starch offers absolutely no nutritional value. It is also an additive in may different products. It’s a processed food. Processed food creates digestive problems.

Condiments

We all love our condiments. They make bland food taste better. We love our dashes of ketchup, mayonnaise, mustard, ranch dressing, sour cream, and also barbecue sauce.

But did you know these tabletop staples are GMO food? They contain high-fructose corn syrup (from genetically modified corn), sugar (from genetically modified sugar beets), and also genetically modified soybean oil. In addition, they have harmful preservatives and additives.

Aspartame

Aspartame is a synthetic low-calorie sweetener in many diet soft drinks, food, and also supplements. Many people who are weight conscious opt to use this instead of regular table sugar.

Metabolic waste products of bacteria produces aspartame. That’s right. The fecal matter of bacteria. And according to the EPA, aspartame also causes neurotoxicity. In addition, recent research shows high carcinogenic effects from the consumption of this GMO food. Not to mention its possible role in non-Hodgkins lymphomas and leukemia.