Iron's Dangers - Ray Peat

Iron's Dangers - and age pigment

One of the major lines of aging research, going back to the early part of this century, was based on the accumulation of a brown material in the tissues known as "age-pigment." The technical name for this material, "lipofuscin," means "fatty brown stuff." In the 1960s, the "free radical theory" of aging was introduced by Denham Harman, and this theory has converged with the age-pigment theory, since we now know that the age-pigment is an oxidized mass of unsaturated fat and iron, formed by uncontrolled free radicals. Until a few years ago, these ideas were accepted by only a few researchers, but now practically every doctor in the country accepts that free radicals are important in the aging process. A nutrition researcher in San Diego suspected that the life-extending effects of calorie restriction might be the result of a decreased intake of toxins. He removed the toxic heavy metals from foods, and found that the animals which ate a normal amount of food lived as long as the semi-starved animals. Recently, the iron content of food has been identified as the major life-shortening factor, rather than the calories. [Choi and Yu, Age vol. 17, page 93, 1994.] 


Become sick – Become a Fruitarian! « by AnthonyColpo

Get to Know Your Local Hospital – Become a Fruitarian! « AnthonyColpo

Get to Know Your Local Hospital – Become a Fruitarian!
Dec 2012 09
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Orthorexia is an eating disorder which involves an obsession for eating a diet based on a restricted selection of food items considered ‘healthy’ by followers. Not only can such dietary habits lead to important nutritional deficiencies, they may cause disturbances in familial and social relationships as others realize you’ve turned into a dietary zealot.

Followers of restrictive regimens especially known for their fanatical behaviour include low-carbers, vegans and fruitarians. The latter feed only on fruits, some using the rationale that our primate ancestors only ate fruit, so therefore we should too. The fact that primates routinely eat vegetation other than fruit, and have been observed to eat meat in the wild and to digest it with full efficiency when studied in captivity never seems to enter the highly dogmatic fruitarian mind.

Other fruitarians believe in non-violence towards plants as well as animals and that we should avoid eating vegetables that are ‘killed’ during harvest such as lettuce, celery or cabbage. Holy cow. If fruits were ‘alive’, I’d say they’d be pretty much screwed at the point where you sink your teeth into them and begin crushing with your teeth. So if ‘killing’ food was a big no-no, then for the sake of consistency those who subscribe to the theory of ‘non-violent’ nutrition should stop eating pretty much everything, except maybe dirt. Or does that have feelings too?

Nope, commonsense has never been a big factor with dietary zealots, and fruitarians are hardly an exception.

But the ‘benefits’ of fruitarianism don’t stop at irrational fanatacism; turns out it’s a great way to get to know your local hospital too!

Researchers from Spain recently described what appears to be the first reported case of ketoacidosis secondary to starvation in a frutarian patient[1]. A 35 year old male with a history of three previous admissions to psychiatric units was brought to the Emergency Room via ambulance, presenting with behavioural disturbances, including aggressiveness and voluntary complete fasting for over a
week. In the last 10 years, the patient had progressed from a lacto-ovo vegetarian diet to one consisting solely of fruit.
On presentation, the patient was clearly ill, displaying psychomotor impairment and incoherent speech. He had a body mass index (BMI) of 16, and urinalysis was positive for ketone bodies (>150 mg/dl). Protein-calorie malnutrition and vitamin deficiencies (folate and vitamin D) were evident. He was treated with intravenous glucose, insulin, vitamins and minerals.

The patient’s motivation for eating only fruits was based on the desire to avoid harming animals and vegetables. He only allowed himself to eat fruit because it was produced by a plant, and consumption of the fruit did not kill the plant (hang on a minute; dairy and egg consumption doesn’t kill the source animals, so…oh I forgot, this article is about irrational dietary zealots).

As if that weren’t loopy enough, the patient refused to receive tube feeding claiming that “receiving enteral nutrition won’t allow him to follow his dietary habit”, necessitating IV parenteral nutrition with supplemental phosphate, potassium, calcium and magnesium.

A psychiatric consult was requested, and a diagnosis of “undetermined psychotic disorder” was given. I told you these jokers are crazy…

The patient’s week of strict voluntary fasting prior to admission was considered most likely the cause of ketoacidosis. Initially, the presence of ketonemia and low glucose levels ruled out diabetic ketoacidosis as the cause, and negative laboratory results for toxicology and alcohol levels further implicated starvation as the aetiology of the acid-base imbalance. Ketoacidosis secondary to starvation is due to diminished insulin secretion, leading to an increase in ketogenesis. The big irony here is that vegan/fruitarian proponents routinely attack meat for its alleged acidic properties, and attack the ketotic state of their low-carb rivals as unhealthy.

What I personally find really, really sad here is that this happened in Spain. I mean, c’mon’…Spanish blokes eating fruitarian diets? What next? Italian blokes listening to Abba and drinking soyaccinos? What’s happening to people, for crying out loud?

Wake Up and Smell the Bullshit, Folks

The above case report reminds me of a certain emaciated fruitarian who loudly wanks on and on about how wonderful his diet is, but for some strange reason never mentions the time he was admitted to hospital a few years back in a very non-wonderful state after eating nothing but bananas for 2 weeks straight. He has since expanded his dietary repertoire to include mangoes, dates and – in keeping with his 100% natural, all-organic philosophy – synthetic B12 injections, which of course were widely used by our primate ancestors.

It also reminds me of an email I received a month ago from a lad in the Netherlands, asking for advice on how to repair the severe damage he’d done to himself after an extended bout of fruitarianism. Here’s the guts of his email, edited for brevity:

“I am 20 years old, live with my parents in the Netherlands, and, after nearly being dead and still being relatively weak, currently have no job or money to pay you for advice…My situation put very, very briefly is this: I ate a diet consisting of nothing but fruit for 6 months, lost my libido, body hair, got a diastolic blood pressure of 35, was so weak I could not walk to the end of the street anymore -> Went to a GP, got diagnosed panhypopituitarism and was put on HRT for thyroid hormone, growth hormone, testosterone and cortisol -> Went to an endocrinologist, got misdiagnosed again -> Found out about the fact that I was misdiagnosed and that diet, rather than a malfunctioning pituitary gland caused my problems and discussed this with the endocrinologist -> Will now get regular check-ups on hormone levels and slowly wean off the HRT, I am also under the guidance of a dietitian, who put me on a 2100 kcal diet with macro’s C/F/P 50/30/20. I was luckily able to choose what foods to eat, staples are red meat/potatoes/rice/eggs.

I am an ex-hobby- bodybuilder, at my peak I was 71 kg@8%@1.71(BP 125, SQ 145, DL 180). Right now, I am 59 kg@13%%1.71(BP 70, SQ 55, DL ??), have got the testosterone levels of an average female and have yet to wean off of hydrocortisone and thyroid hormone (am on full replacement dosages for both). Within the next weeks I will get bone density tests and a decent BF% measurement. I have been binge eating for the last three weeks, that’s how I went from the 7% I am on my profile picture, to about 13% in a very short time while not really gaining any muscle or strength, sad, but I have to live with it.

I desperately want to get back to 7%, but recovery of my hormonal health obviously has priority, at the hospital, the did not want me to go low bodyfat, especially not now.”

For heaven’s sake. Why do people fall for this nonsense? What is it about the human species that makes people so dopey and gullible they’ll readily believe eating nothing but fruit is a smart thing to do? Humans have been eating animal flesh, tubers, and other assorted forms of vegetation for millions of years – deal with it, folks. And realize that without these foods, we wouldn’t even be here today. Instead we would have been emaciated fruitarians too weak to fight off and flee from sharp-toothed prey, and too infertile, impotent, amenorrheic and nutrient-depleted to successfully pass on our genes (no enteral IV drips back in the Stone Age, folks…)

PS: I’ve just learned that Matt Stone has been conversing with the above Dutch ex-fruitarian, and has presented a more detailed – and alarming – report on this young lad’s diet and health history. It should be mandatory reading for anyone tempted by the trendy but harebrained intermittent fasting, zero-carb and fruitarian fads: http://180degreehealth.com/2012/10/fat-loss-secret


1. Causso C, et al. Severe ketoacidosis secondary to starvation in a frutarian patient. Nutr Hosp, 2010; 25 (6): 1049-1052.

View the free full text here: http://www.nutricionhospitalaria.com/pdf/4905.pdf

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of the groundbreaking books The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.


low vitamin D levels may be a consequence, not a cause, of poor health

Why I don’t take vitamin D supplements /  Getting Stronger

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Posted 11 Nov 2012 in Uncategorized

Vitamin D has been associated with numerous health benefits, including cardiovascular and immune health, bone strength, and prevention of cancer. However, studies claim that most of us are deficient in vitamin D, and thereby unnecessarily vulnerable to increased heart disease, stroke, cancer, diabetes, osteoporosis, infection and autoimmune disorders.  According to a review of recent studies in Natural News, there is a woldwide epidemic of vitamin D deficiency:  59% of the population is “vitamin D deficient”.  The article goes onto to speculate that “What’s becoming increasingly clear from all the new research is that vitamin D deficiency may be the common denominator behind our most devastating modern degenerative diseases.”

Supplementation with vitamin D capsules is advocated even by “primal” advocate  Mark Sisson, normally one to take inspiration from our paleolithic ancestors, shunning medication and embracing a lifestyle of eating whole foods and engaging in moderately stressful, playful exercise:
We can’t all bask in the midday sun.. For those of us unable to run shirtless and shoeless through a sun kissed meadow…our option is oral intake… food will help, but it won’t suffice. You need something stronger. ..take a good D3 supplement if you can’t get real sunlight. As long as you don’t go overboard on the dosage, you’re good to go. If it’s not in an oil-based capsule, just take it with a bit of fatty food (not a stretch for an Primal eater). It travels the same pathway and results in the same benefits. It’s always easier to just let nature take its course, but it’s not always realistic. A good general rule is 4000 IU per day.
Therefore, we should supplement with vitamin D.  Right?

Not so fast.  A closer examination shows that low vitamin D levels may be a consequence, not a cause, of poor health.  And that supplementation with Vitamin D may actually be counterproductive.  Let me explain.

Homeostatic regulation.  First, I’d like to return briefly to a previous post I wrote.  In The case against antioxidants, I presented evidence that supplementation with antioxidants is not only unhelpful, but may actually be counterproductive.  In my article, I surveyed several meta-analyses of  the antioxidant vitamins A, C, and E — demonstrating a lack of benefit from supplementation, and in some cases positive harm.  At first, this result surprised me. How can one explain it?  After all, we know that vitamin-rich fruits, vegetables and herbs are good for us.  Extracts from these anti-oxidant-rich foods have been shown to neutralize reactive oxygen species (ROS) in the lab.  Hence, it must be the case that fruits, vegetables and herbs are good for us because of their antioxidant content – right?
Wrong. As we all know, correlation does not always imply causation.  And it turns out that fruits, vegetables and nuts may improve our resistance to oxidative damage for reasons other than their antioxidant content.

A more likely reason is that these foods are rich in polyphenolic phytochemicals–such as bioflavanoids– that stimulate the cells in our bodies to turn on a transcription factor called Nrf2, which activates our “xenobiotic” defense system.  This xenobiotic defense system or Antioxdiant Response Element turns on the production of a number of  endogenous anti-oxidant enzymes–such as superoxide dismutase and glutathione peroxidase–that inactivate ROS species catalytically.  That means that unlike the antioxidant chemicals in foods–which quickly get used up one-for-one when neutralizating oxidant molecules–the anti-oxidant enzymes turn over thousands of times, and are thus far more potent and sustainable defenses.  In addition, these enzymes are produced in cells throughout the body, localized where they are needed most.

In short, empowering our in-born antioxidant defense system is much more effective than supplementing with chemical antioxidants.

But what is even more startling is that supplementing with endogenous antioxidants can actually suppress your body’s endogenous ARE defense system.  Startling, but not too surprising once you realize that the ARE system is homeostatically regulated. That means that your metabolism compensates for external changes by making the appropriate internal changes in order to restore a rough balance.   Just as body temperature, blood glucose, and countless other internal variables are regulated, our defenses against oxidative stress are regulated.

Homeostatic regulation, ubiquitous in biology, evolved to help us adjust to changing circumstances, and to conserve resources. If antioxidants are supplied from the outside, there is less need to spend energy and internal resources making our own anti-oxidant enzymes, so the organism turns town their production.  In my earlier article, I surveyed studies showing that this is just what happens, concluding:
So it appears that, by consuming more antioxidants, we become dependent upon them and perversely reduce our innate ability to detoxify. With any let-up in the constant supply of external defenses, we become more vulnerable to oxidative and inflammatory attack. And the externally supplied antioxidants themselves are in any case much less effective than the endogenous ones.
I ended by recommending that we select foods and herbs not for their anti-oxidant content, but rather for their hormetic ability to stimulate our native ability to produce’s its own detoxifying antioxidant enzymes.  At the top of that list are brightly colored and bitter foods and herbs, such as broccoli, blueberries, red peppers, curcumin, green tea and even chocolate.

The moral of the story:  When possible, build your own capacity rather than relying on external supplies.

Now on to vitamin D.  Not everyone realizes that this “vitamin” is actually a hormone — a secosteroid in the same family as other steroid hormones like testosterone and cortisol.  As a hormone, the primary function of vitamin D is to regulate levels of calcium and phosphorus in the bloodstream, thereby promoting healthy bone formation.  But vitamin D also regulates a number of other important processes in the body, such as activation of both the innate immune system and the adaptive immune system.

The diet can supply vitamin D as either D2 (ergocalciferol, from plants) or D3 (cholescalciferol, from animals), but it is most effectively synthesized in the skin by the action of UV-B rays in sunlight acting on 7-dehydroxycholesterol.  (Yes, it all starts with cholesterol!).  But neither D2 nor D3 — the molecules present in supplements or food — are biologically active forms of the vitamin.  The diagram at right shows how vitamin D must first be converted by hydroxylation to calcidiol (usually designated as 25 (OH) D, or just “25-D”) in the liver and then further hydroxyulated to calcitriol (1,25 (OH)2 D or just “1,25-D”) in the kidney.  It is the 1,25-D form that is biologically active, binding to the vitamin D receptor (VDR) and activating a cascade of important biological functions, such as calcium absorption in the intestines.  So a well-functioning liver and kidney are required in order for vitamin D to be effective.

Vitamin D studies. Nobody doubts the important role of vitamin D in the body.  But are higher levels of a hormone like vitamin D–whether or not provided as a supplement– always a good thing?  Well, that is far from clear.  In a review of vitamin D studies in The End of Illness, David Agus, professor of medicine at University of Southern California, cites both positive and negative consequences of increased vitamin D levels.  On the positive side, a 2009 study presented by the Intermountain Medical Center in Utah, following 27,686 men older than 50 years over the course of a decade, found that those with the lowest levels of vitamin D had:
  • 90% higher incidence of heart failure
  • 81% higher incidence of heart attack
  • 51% higher incidence of stroke
Pretty impressive association!  And yet Agus also cites two negative studies worthy of comment:
  • A 2010 double-blind, placebo-controlled study, published in the Journal of the American Medical Association, found that older women who received annual oral high-dose vitamin D had an increased risk for falls and fractures.
  • A 2008 study, published in the Journal of the National Cancer Institute, found that vitamin D does not reduce the risk of prostate cancer, and furthermore that higher circulating levels of 25-hydroxyvitamin D may be associated with an increased risk of more aggressive forms of prostate cancer.
Correlation vs. causation.  Agus points out that most of the vitamin D studies are “observational studies” that show associations. They uncover a correlation bertween vitamin D levels and some other condition. But they don’t show cause and effect. The few mechanistic studies of vitamin D action were mostly carried out in cell culture, for example adding vitamin D to breast cancer cell cultures suppressed their growth.  But in real humans, vitamin D is part of a homeostatic regulation system.  Vitamin D doesn’t just do one thing, like promote bone growth.  It is involved in as the regulation of as many as 2000 genes, turning up the expression of some, turning down the expression of others.
So how do we interpret these associations? As Agus points out, in regard to the Utah study:
An association, however, does not prove cause and effect. Another way of looking at this study is to say it’s quite possible that a heart condition lowers vitamin D levels, directly or indirectly— by keeping people with health challenges indoors and out of the sun. Also, obesity throws another wrench into the problem because excess fat absorbs and holds on to vitamin D so that it cannot be properly used in the body. Hence, is low vitamin D in this study just a marker for those who were obese? It’s the old chicken-and-egg conundrum. The same can be said for hundreds of other such studies that link the health (or lack thereof) of an individual to levels of vitamin D.
This is the key point:  Low vitamin D levels may be a biomarker for other problems.  It may be the consequence, rather than the cause, of certain conditions such as heart disease or obesity. For the same reason, high vitamin D levels may be a biomarker for good health.  Agus quotes Dr. JoAn Manson, chief of preventive medicine at Brigham and Women’s Hospital:
People may have high vitamin D levels because they exercise a lot and are getting ultraviolet-light exposure from exercising outdoors. Or they may have high vitamin D because they are health conscious and take supplements. But they also have a healthy diet, don’t smoke, and do a lot of the other things that keep you healthy.
If vitamin D level in the blood is merely a biomarker, a consequence of good or bad health, then adding vitamin D to the diet will not necessarily improve your health.  To really know whether vitamin D supplementation is beneficial, we need to look at interventional studies, where supplements are provided, and the outcomes are compared with those of control subjects who don’t get the supplement.  In fact the two above-cited studies on the effects of supplementation on bone fractures in older women, and prostrate cancer in older men are two such interventional studies.  And they showed that vitamin D supplementation was harmful in both cases.  And note that the positive Utah study I cited above–showing a correlation between low vitamin D levels and elevated incidence of cardiovascular disease and stroke–was an observational study, not an interventional one.

The men in that study with the higher vitamin D blood levels and lower incidence of heart disease were not given supplements.

Vitamin D levels are homeostatically regulated in our bodies, and this process varies with your genetics and health.  As one examlple of this, people with lighter skin color and less melanin in the skin evolved to make higher vitamin D levels even with reduced sun exposure; the converse is true of those with darker skin. (This may explain why African Americans are at much higher risk for vitamin D “deficiency”, particularly if they live in higher latitudes and work indoors).  People vary widely in the level at which they regulate vitamin D levels in their blood — it tends to be homeostatically controlled in a given individual, but the “normal” level may vary between 8 and 80 ng/ml, or even more widely than that.  Vitamin D levels are are genetically controlled by 3 or 4 genes, and are under control of the vitamin D receptor.  (This homeostatic regulation of vitamin D levels will sound familiar to those who read my previous post, “Change your receptors, change your set point“).  As Agus notes,
When your cells are deluged with vitamin D…they will pull back on their sensitivity to vitamin D by reducing their number of receptors for vitamin D. But if there’s a perceived shortfall of vitamin D in the bloodstream, your cells will up-regulate— create more receptors for vitamin D— to become more sensitive to every vitamin D molecule that passes by. What happens, then, when we consume lots of vitamin D from unnatural sources such as supplements? (I use the term unnatural to imply that it’s not coming from the sun, which is a source of vitamin D that has built-in regulatory mechanisms.) No doubt our bodies are adept at adjusting using their feedback loops as I just described, and the constant surplus of vitamin D means our cells are constantly down-regulating. If we took the supplemental vitamin D away, our cells would up-regulate to make up the difference. Vitamin D has multiple downstream signaling molecules, for the vitamin D receptor signals several reactions.
So if you take vitamin D supplements, and vitamin D is regulated homeostatically, your body will turn down its endogenous production of vitamin D.  If you believe that vitamin D is a “biomarker” of good health, do you really want to turn down the upstream processes that synthesize vitamin D?  Think about that before you pop a vitamin D capsule.

Unintended consequences.  Even worse, taking vitamin D supplements may actually suppress the immune system.  This “alternative hypothesis” of vitamin D has been put forward by Trevor Marshall and Paul Albert.  Supplementation with vitamin D will tend to increase levels of the inactive form of vitamin D–that is,  25-D.  Conversion of inactive 25-D to active 1,25-D in the kidneys is not immediate, and may not be efficient, particular if kidney function is less than optimal.  Now here is the problem:  While both the inactive 25-D and active 1,25 bind to the  vitamin D receptor (VDR), only the 1,25-D turns on the VDR, allowing it to perform its beneficial functions; the inactive 25-D actually inhibits the VDR.  This is a problem because the VDR is the “gate-keeper” of the innate immune system, regulating over a thousand genes. So elevated levels of 25-D can result in immunosuppressive effects.  As Albert writes in Vitamin D: The alternative hypothesis:
Indeed, the secosteroid 25-D may exert palliation on the innate immune system not unlike the way corticosteroids exert palliation on the adaptive immune system. So is it possible then that supplemental vitamin D is now perceived as a wonder substance simply because it effectively palliates the inflammation associated with diseases across the board? If so, this would certainly explain why its effects are most noticeable in the short-term and why efficacy often diminishes in the long-term.
And we need to also take into account the regulation of vitamin D levels through homeostatic feedback processes.  Consider that it is typically the 25-D form of vitamin D–not the biologically active 1,25-D– that is measured in blood tests.  And there is very little correlation between the active and inactive forms, as shown in the the figure below, from a 2009 study by Blaney et al., published in the Annals of the New York Academy of Sciences in a sample of 100 Canadian patients. As the authors note, while  many of the subjects had very low levels of 25-D–the type reported in most blood tests–most of them had levels of 1,25-D elevated above the normal range. Can those subjects with low levels of 25-D but elevated levels of the biologically active 1,25-D truly be considered vitamin D deficient?
Because low levels of 25-D are often associated with inflammatory conditions such as cardiovascular disease and autoimmune disease, people jump to the conclusion that low 25-D levels are a cause of the inflammatory condition.  On this point, listen again to Albert:
Yet, the alternative hypothesis must be considered – that the low levels of 25-D observed in patients with chronic disease could just as easily be a result rather than a cause of the inflammatory disease process. Our research suggests that this is the case. Indeed we have found that 1,25-D tends to rise in patients with  chronic disease and that these high levels of 1,25-D are able to downregulate through the PXR nuclear receptor the amount of pre-vitamin D converted into 25-D, leading to lower levels of 25-D.  I describe this finding further in my paper.  So are we really facing an epidemic of vitamin D “deficiencey” or are we simply beginning to note more signs of an imminent epidemic of chronic disease – an epidenmic which would be exacerbated by increasing the amount of vitamin D added to our food supply?
So the body is making enough active vitamin D to deal with inflammation–maybe even too much, leading to downregulation of the inactive 25-D precursor.  Trevor Marshall has also pointed out that elevated levels of 1,25-D may result from impaired activity of the  VDR, which is essential for innate immunity.  The excess 1,25-D can cause problems with other secosteroid receptors in the body, such as the thyroid receptor.  But adding more 25-D, beyond what is needed, will tend to only further inhibit the VDR, interfering with its beneficial anti-inflammatory actions, and impairing innate immunity.  In other words, well-intended supplementation with Vitamin D3 may actual backfire. Something to think about!

Marshall is currently conducting studies with a protocol involving restriction of vitamin D and use of an agonist drug that binds to the VDR receptor, upregulating it, and acting as an immuno-stimulant to treat immune disorders like arthritis and multiple sclerosis.  Marshall’s protocol is controversial, because it flies in the face of the orthodoxy about Vitamin D.  He acknowledges that vitamin D supplementation can indeed deliver some short term benefits because it acts as an immuno-suppressant–in much the same was as corticosteroids like prednisone. But just as prednisone is useful for acute treatments, yet is harmful if taken chronically, the immune-suppresant effects of vitamin D on the VDR may be detrimental.

One need not go to the extent of restricting or avoiding vitamin D to exercise some caution about actively supplementing it.  If supplementation has risks, is there anything you can do to ensure adequate levels of the active form of vitamin D?  Certainly, it is important to have at least an adequate level of D3 entering the liver, by eating foods rich in vitamin D,  and through biosynthesis from adequate exposure to sunlight.  But you also want to make sure that the conversion processes to 25-D in the liver and 1,25-D in the kidneys are functioning well.  Which means eating a low-inflammatory diet — that is, one that is low in sugars, processed omega-6 vegetable oils and other pro-inflammatory compounds.

Here is the takeaway from this vitamin D story, together with my earlier post about antioxidants: Inflammatory conditions, such as heart disease, infection or autoimmune disease are often associated with reduced levels of certain biomarkers in the blood,  such as antioxidant vitamins or hormones.  Our natural instinct is to conclude that these are “deficiencies” that need to be corrected.   While that may sometimes be the case, particularly in extreme cases, you should keep in mind the direct supplementation with additional vitamin or hormone may actually be counterproductive–by shutting down or impairing your body’s own ability to mount it’s own defense against oxidative stress and inflammation.

Rather than taking hormone and vitamin supplements, it is more effective to stimulate your body to strengthen its own defense and detoxification systems.  I’m not against all supplementation — for example, I believe that ingestion of phytochemical-rich vegetables and herbs is useful as a hormetic stimulus.  But I think we have to overcome the simplistic notion that if X is a good thing, we should consume more of X.

The body is more than a repository for chemicals — it is a self-regulating organism with hundreds of complex and dynamic feedback loops, evolved to enable us to adapt to changing circumstances and meet many challenges.  We should take care that what we ingest is used to build up our natural capacities, not subvert them.


Is Alcohol Good or Bad For Health? | Mark's Daily Apple

Alcohol: The Good and the Bad


What do we make of alcohol? In sufficient amounts, it’s a poison. It’s incredibly addictive. It destroys entire communities. It tears families apart and compels otherwise reasonable, upstanding individuals to commit terribly senseless acts. On the other hand, it’s a powerful social lubricant. The good stuff tastes great and can enhance the healthfulness of certain foods while inhibiting the unhealthfulness of others. It’s fun, it’s pleasurable, and it brings real (if chemically enhanced) joy to people. Moreover, we have a long and storied history with alcohol; it’s been an integral part of human culture and society for thousands, if not tens of thousands, of years.

So, what’s the deal? Is it good, or is it bad? Is it poison, or is it a gift? Let’s take a look at both sides of the story, which, as is often the case, isn’t exactly black and white:
First, the downsides.

It’s toxic.

Our ability to break alcohol down into less toxic metabolites didn’t arise because of our tendency to seek out fermented fruits. Over the course of an average day, the average human digestive system produces about three grams of ethanol just from the gut flora fermenting the gut’s contents. If we didn’t have the ability to metabolize and detoxify ethanol, those three grams would add up real quick and represent a huge toxin load on our bodies. After alcohol is consumed, a number of enzymatic reactions ensue. In the liver, an enzyme called alcohol dehydrogenase converts the ethanol to acetaldehyde, an incredibly toxic compound that’s been implicated in causing many hangover symptoms. An enzyme called acetaldehyde dehydrogenase converts the acetaldehyde into acetic acid, or vinegar (which is harmless unless you’re a cucumber). From there, you’re good to go. Sounds simple enough, right? Just let the enzymes do their thing. As long as you make those enzymes, the alcohol will be safely and effectively metabolized into table vinegar which can then be extracted to form a delicious salad dressing (that last part isn’t true).

Unfortunately, not everyone produces the same amount and quality of detoxifying enzymes. Many people of East Asian descent possess a dominant mutation in the gene that codes for aldehyde dehydrogenase, making it less effective. While they’re less likely to be alcoholics, folks with the mutation (characterized by a “flushing” upon ingestion) are at an elevated risk of liver damage and esophageal cancer.

It can give you fatty liver (and worse).

Around these parts, we usually talk about non-alcoholic fatty liver, a disease associated with sugar and fat intake coupled with inadequate choline to support the liver’s function. But notice that we have to qualify it with “non-alcoholic.” That’s because the most-studied type of fatty liver is alcoholic fatty liver. The mechanisms behind alcoholic fatty liver are myriad and multifaceted, but it ultimately comes down to the fact that you’re bathing your liver in a known toxin. Liver alcohol metabolism increases the NADH/NAD+ ratio, thereby promoting the creation of liver fat cells and a reduction in fatty acid oxidation; the result is added fat in the liver and impaired fat burning. Acetaldehyde, especially if it lingers for too long, also induces inflammation in the liver, which can ultimately progress to full cirrhosis and liver failure.

It can be carcinogenic.

Excessive alcohol intake is an established epidemiological risk factor for several cancers, including stomach, liver, and colon cancer (to name just a few; more than a dozen cancers are linked to alcohol abuse). In the stomach and liver, alcohol dehydrogenase converts ethanol into acetaldehyde, which is inflammatory and toxic. Alcohol that makes it through the stomach into the small intestine is also oxidized into acetaldehyde, this time by gut flora. While the liver produces the necessary enzymes to break down acetaldehyde into acetic acid, our gut microbes aren’t so well equipped and the acetaldehyde is allowed to linger longer.

It’s addictive.

While I’d argue that being addicted to anything will have a negative effect on your life, if not your physical health, being addicted to alcohol is particularly harmful because of how toxic it is – especially the more you drink. To get an idea of just how addictive it is, check out the results of this study: alcohol is less addictive than nicotine, crystal meth, and crack, but more addictive than heroin, intranasal amphetamine, cocaine, and caffeine. One’s susceptibility to alcohol addiction is often hereditary, too, meaning some people will be far more likely to become addicted than others.

It disrupts sleep.

A nightcap is a misnomer. Sure, it’ll help you fall asleep, but your sleep won’t be any better. In fact, as plenty of people reminded me in the comment section of last week’s post on sleep, alcohol is a serious disrupter of sleep quality. It increases the incidence of sleep disruptions, and it perturbs the healthy sleep cycles.

It affects judgment and perception.

Even though alcohol destroys a person’s ability to safely maneuver a motor vehicle, one in three car accidents that result in death involve drunk drivers. Everyone knows that you shouldn’t drive drunk, but why does it keep happening? A recent study even showed that just a single drink caused subjects to find “intentionality” in other people’s actions (PDF). Subjects who got the alcohol were less likely to view simple actions as accidental, rather than intentional. Thus, when you’re under the influence of alcohol, you’re more likely to take personal offense at the guy bumping into your shoulder, the lady stepping on your shoe, or the person “staring” at you from across the bar. Because, after all, they “meant” to do it, right? The title of the study sums it up quite nicely: “‘There’s No Such Thing as an Accident,’ Especially When People are Drunk.”

It promotes bad eating.

Everyone who’s ever gotten at least a buzz from a glass or two of wine or a mixed drink has felt the often irresistible urge to snack, to order something salty, crunchy, and sweet from the menu, to beg the driver to swing by the greasiest nastiest fast food drive-thru. This is a well-documented phenomenon. Alcohol affects both active overeating and passive overeating. Active overeating describes the conscious decision to “get some grub.” Passive overeating describes the amount you eat once the food is in front of you. Both are enhanced by alcohol. This wouldn’t be such a bad thing if you’re drinking at a Primal meet-up, where you’re surrounded by relatively healthy food, but that’s not where most drinking occurs.

It gives hangovers.

What’s worse than a bad hangover? I’m unaware of anything, at least on a physical scale. Sure, you can mitigate the damage, but the fact that a hangover even exists tells us that whatever we’re ingesting that gave us the hangover is bad for us (in the amount we ingested, at least).
But what about the positives?

It improves endothelial function (with a catch).

Impaired release of nitric oxide from the endothelial cells is strongly associated with cardiovascular disease. Ethanol actually increases the production of nitric oxide, which dilates blood vessels, regulates blood pressure, induces vascular smooth muscle relaxation, and basically improves endothelial function. If you want good cardiovascular health, you want good endothelial function. However, it’s important to note that large doses of ethanol seem to decrease endothelial function, so caution is obviously warranted.

It can reduce stress.

A lot of people use a glass of wine or beer to “wind down” after a hard day. This sounds bad on the surface – “you’re relying on alcohol to stay sane!” – but really, if you have to choose between stewing in your stress hormones all day and night and having a drink or two to settle yourself down, I think the drink can be a better option for some people – particularly if the stress is going to impair your sleep and affect your relationships. You’ll want to identify and deal with the original source of the stress, of course, but some people may find a net benefit from having that drink.

It promotes socializing.

Humans are social animals, and we are happiest and healthiest when we have friends, loved ones, and spend quality time with them. Social isolation is a consistent and strong risk factor for increased mortality and morbidity (meaning it’s linked with earlier death and worse health in the days up until that death). You shouldn’t base your socialization entirely on drinking alcohol, but it can certainly be a powerful enhancer of your social life, and if you’re having a couple of glasses of wine as you host dinner parties, hang out with friends, enjoy a candlelit dinner with your significant other, or throw a BBQ with your social circle, it will likely have a net positive effect on your health. Of course, this isn’t to say that alcohol is any way needed to have a good time in a social setting.

It can reduce post-prandial blood sugar and lipid peroxidation (when taken with a meal).

Just like it says above, drinking alcohol (like wine, for example) with food can reduce postprandial blood glucose and the susceptibility of blood lipids to peroxidation (PDF).

It can lower iron absorption if you’ve got iron overload.

Although the conventional push is to increase the intake of iron from foods (especially via fortified grains), some people don’t actually need the added iron. If you have hemochromatosis, a genetic condition that probably arose in Europeans as a survival response to the bubonic plague, you are a hyper-absorber of dietary iron. Luckily, ethanol seems to inhibit the absorption of heme iron, the kind you find in red meat. Red wine is also effective at reducing non-heme iron absorption, an effect most likely due to the polyphenols present. That said, the entirely non-alcoholic black tea also inhibits iron absorption and has even been shown to reduce the frequency of blood-draws required in patients with iron overload. Coffee works, too.

If you’re going to drink:

Have it with food.

When you eat a meal, and your stomach is “full,” the pyloric sphincter – which controls the passage of food and drink from the stomach into the small intestine – closes up until your stomach can break down its contents. Any alcohol added to a full stomach will also spend more time being broken down by the relevant enzymes. If you drink on an empty stomach, the pyloric sphincter is wide open, and a greater proportion of alcohol will make it to the small intestine for immediate absorption. Plus, as I mentioned earlier, drinking alcohol with food can reduce postprandial blood glucose and the susceptibility of blood lipids to peroxidation (PDF). Keeping your drinking around meals will let you take advantage of these benefits.

Focus on alcoholic drinks with greater fluid content.

Shots of plastic bottle vodka (or even the best vodka) are concentrated sources of ethanol, and as long as we’ve been nibbling on fermented fruits and brewing up Paleolithic moonshine from mushrooms and honey, consuming concentrated, distilled ethanol in the form of rum, gin, whiskey, vodka, and other hard liquors is a relatively recent practice. Some accounts suggest that the Chinese were distilling rice liquor in 800 BC, while others say it wasn’t until the 12th century AD that distillation became commonplace across the “known” world. At any rate, one could certainly argue that alcohol with a low fluid content is an evolutionarily novel food item. Less fluid means less “stuff” in your stomach, which means a more open and allowing pyloric sphincter, which means faster absorption through the small intestine. More fluid means more “stuff” in your stomach and a more restrictive pyloric sphincter and slower absorption. You could even make like the ancient Greeks and water down your wine, which some people seem to think actually improves the wine.

Choose your drinking companions wisely.

Even among voles, peer pressure-induced binge drinking is a reality. If that super cool vole with the sweet facial hair is double fisting acorn shells filled with dandelion wine, you’ll be subconsciously drawn to do the same. If your group of friends gets absolutely obliterated every time you go out with them, you’re more likely to join in on the “fun.”

Drink moderate amounts.

All the research suggesting health benefits to drinking revolves around “moderate drinking,” which is one, two, or three drinks a day. They’re not talking about pounding shots, or drinking Long Island iced teas, or doing Jello shots (although the gelatin might help matters). They’re talking about a glass or two of something.

Have everything else in line.

If you want to drink and remain healthy, you should strive to eat healthy, exercise well, reduce stress, walk a lot, experience nature, hang out with friends and loved ones, get sun when available, avoid nighttime light exposure as much as possible, and every other lifestyle prescription I recommend. In short, alcohol can augment (or at least fail to impact either way) an already healthy lifestyle, but it probably won’t make a bad situation better.

Full disclosure: I drink. My drink of choice is red wine, and I might do a glass or two most nights, but I never get drunk. Heck, I don’t even really get “buzzed.” I’d never recommend that people take up drinking or continue drinking, but I also don’t see it as a great evil in and of itself. The dose and frequency make the poison; it’s just that depending on a number of factors, the dose that makes alcohol a poison might be lower or higher for you than for me. If your sleep is affected or you are the least bit “off” the next day, you probably surpassed your ability to effectively process it and you should factor that in to your choice and approach to drinking again. And remember, alcoholism is a serious issue for some people and I am in no way suggesting there is any “workaround” or excuse herein for someone with those issues, or that drinking, even in moderation, is necessary or optimal for healthy living.

Okay, that’s about it for me. Let’s open it up to you guys, now. I want to hear your thoughts on alcohol, especially whether it’s had a positive, negative, or neutral effect on your life and the life of those you care about. I want to hear how you’ve integrated alcohol into your otherwise healthy lifestyle (or not). Thanks for reading!

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Eating fish safe - A lot safer than not eating fish!

Is eating fish safe? A lot safer than not eating fish!

This is going to be a long article and I know not everyone will have time to read it. So I’m going to summarize the key points right up front because I think this information is so important:


  • Selenium protects against mercury toxicity, and 16 of the 25 highest dietary sources of selenium are ocean fish
  • If a fish contains higher levels of selenium than mercury, it is safe to eat
  • Most species of commonly eaten fish in the U.S. have more selenium than mercury
  • Fish are not significant sources of PCBs and dioxins when compared to meat, dairy or vegetables
  • The benefits of eating fish regularly far outweigh the potential risks, which are neglible
  • Pregnant mothers and young children should eat 2-3 servings of oily ocean fish each week
These days a lot of people are scared to eat fish. They’ve been told that fish are full of contaminants like mercury, PCBs and dioxins that cause neurological problems and may increase the risk of cancer. Pregnant women have been especially warned due to the supposed risk of these toxins to the developing fetus.

In the last few articles I’ve established the importance of the long-chain omega-3 fatty acids EPA and DHA in human health. I’ve argued that the conversion of plant-based omega-3 fats like ALA into the longer chain EPA and DHA is extremely poor in most people.

The conclusion is obvious: fish should be a part of our diet. But is it safe to eat fish?

You might be surprised to learn that the answer is a resounding yes. In this article I’ll demonstrate that concerns about toxins in fish have been overblown, and that there is almost no risk associated with eating fish when a few simple precautions are taken.

The selenium story

Although people are increasingly concerned about the effects of mercury levels in fish, recent evidence suggests that the trace amounts of mercury in the fish Americans eat aren’t high enough to pose a health risk.

But measuring only mercury significantly exaggerates this risk, because it ignores the important role of selenium.

Selenium is plentiful in many ocean fish species, but the public is unaware of its protective role against mercury. Selenium has high binding affinity for mercury. This means that when the two elements are found together, they connect, forming a new substance.

This new substance makes it hard for the body to absorb the mercury separately. Simply put, when selenium binds to mercury, mercury is not longer free to bind to anything else – like brain tissue.
Studies have shown that relevant amounts of selenium (Se) can prevent oxidative brain damage and other adverse effects associated with mercury toxicity. (PDF)

University of North Dakota researcher Nicholas Ralston has published several papers on the protective effects of selenium. He describes the relationship between selenium and mercury as follows:
Think of dietary selenium as if it were your income and dietary mercury as if it were a bill that you need to pay. Just as we all need a certain amount of money to cover living expenses such as food and rent, we all need a certain amount of selenium.
And guess what foods are highest in selenium? You’re right! 16 of the 25 best sources of dietary selenium are ocean fish.
He goes on:
Only one major study has shown negative effects from exposure to mercury from seafood, and that seafood was pilot whale meat. Pilot whale meat is unusual in that it contains more mercury than selenium. When you eat pilot whale meat it’s like getting a bill for $400 and a check for less than $100. If that happens too much, you go bankrupt. On the other hand, if you eat ocean fish, it’s like getting a check in the mail for $500 and getting a bill for $25. The more that happens, the happier you are.
What Ralston is telling us is that as long as the fish we’re eating has more selenium than mercury, there’s nothing to worry about.

Fortunately, studies by several independent organizations have consistently shown that most of the fish we eat contain significantly more selenium than mercury. Fish that contain more mercury than selenium include pilot whale, tarpon, marlin, swordfish and some shark.

The following chart illustrates the relative levels of selenium and mercury in commonly eaten ocean fish:

The selenium health benefit value (SeHBV)

Researchers have proposed a new measure of seafood safety called the Selenium Health Benefit Value (SeHBV) that takes the protective role of selenium into account.

Fish with a positive (above zero) SeHBV ratio would be safe to eat, whereas fish with a negative ratio would be unsafe. Using these criteria, most varieties of ocean fish have positive SeHBV ratios and are thus safe to eat.

A study conducted by the Energy & Environmental Research Center (EERC) and the Environmental Protection Agency (EPA) also found that an estimated 97% of the freshwater fish from lakes and rivers in the western U.S. are safe to eat. It is the only study I’m aware of that has measured both mercury and selenium levels in the tissues of freshwater fish. 1

So how much fish is safe to eat?

The joint recommendation for fish consumption of the EPA and FDA as of 2004 is as follows:
  • Eat up to 12 ounces (2 average meals) a week of a variety of commonly eaten fish and shellfish found consistently low in mercury, including shrimp, canned light tuna, salmon, pollock, and catfish
  • Limit albacore tuna to 6 oz. per week
  • Do not eat shark, swordfish, king mackerel, or tilefish because they contain high levels of mercury
Notice that these recommendations are already quite liberal compared to the fish-phobes who suggest we avoid fish entirely.

But even these recommendations are too strict, because they don’t take the protective effects of selenium into account. As long as the fish is higher in selenium than it is in mercury, there’s no reason to limit consumption to 12 ounces per week.

What about dioxins and PCBs?

PCBs are synthetic organochlorine compounds previously used in industrial and commercial processes. Dioxins are organochlorine by-products of waste incineration, paper bleaching, pesticide production, and production of certain plastics. Yummy!

While it makes perfect sense to try to avoid these toxins to the greatest extent possible, abstaining from fish isn’t a particularly good strategy.

The highest dietary sources of PCBs and dioxins are not fish, but beef, chicken and pork (34%), dairy products (30%) and vegetables (22%). Fish constitute only 9% of our dietary intake of these chemicals.
The primary concern with PCBs and dioxins is cancer. Animal studies and some evidence in humans suggest that both are carcinogenic.

However, an analysis has shown that, per 100,000 individuals, consumption of farmed vs. wild salmon would result in 24 vs. 8 excess cancer deaths, respectively, while consumption of either farmed or wild salmon would result in 7,125 fewer coronary heart disease (CHD) deaths.

Another analysis of the same data suggested that, for all ages evaluated (25-35 to 85 years), CHD benefits outweighed cancer risks by 100- to 370-fold for farmed salmon and by 300- to more than 1000-fold for wild salmon.

It’s important to note that the benefits of fish consumption are based on prospective studies and randomized trials in humans, whereas estimated cancer risks include a 10-fold safety factor and are based on experimental data in animals and limited studies in humans at extremely high doses.
Cancer estimates also assumed lifetime salmon consumption of 1,000 mg/d of EPA & DHA (four 6-oz servings of wild salmon every week for 70 years). Of course virtually nobody in the U.S. currently eats this much salmon.

On the other hand, CHD mortality reduction may be achieved with lower intake (i.e. 250 mg/d – one 6-oz. wild salmon serving per week). At this intake, CHD benefits would be the same (7,125 fewer deaths) while lifetime cancer risk would decrease by 75% (6 and 2 estimated deaths per 100,000 for farmed and wild salmon respectively). The CHD benefits would outweigh cancer risks by more than 3500-fold in the case of wild salmon.

Once again, with few exceptions (the species of fish with more mercury than selenium), it’s not only safe but incredibly beneficial to eat fish regularly.
How beneficial? Let’s find out.

Fish consumption, cardiovascular disease and total mortality

In 2006 Mozaffarian & Rimm published a paper in JAMA called “Fish Intake, Contaminants and Human Health: Evaluating the Risks and Benefits“. They analyzed several studies that examined the impact of fish consumption on both coronary and total mortality. They found that modest fish consumption (e.g. 1-2 servings/wk) – especially of oily fish higher in EPA and DHA – reduced the risk of coronary death by 36% and total mortality by 17%, and may favorably affect other clinical outcomes.

The authors summarized their findings this way:
For major health outcomes among adults, based on the strength of the evidence and the potential magnitudes of effect, the benefits of fish exceed the potential risks.
For women of childbearing age, benefits of modest fish intake, excepting a few selected species, also outweigh risks.
They also pointed out that the Japanese eat 900 mg/d of EPA & DHA on average, and have death rates from coronary heart disease 87% lower than those in Western populations (like the U.S.).

If you’re interested in learning more about this study, I recommend listening to the JAMA Audio in the Room interview with its lead author, Mozaffarian.

Fish consumption, pregnant mothers, and children

DHA is essential for proper development of the brain. It is preferentially incorporated into the rapidly developing brain during gestation and the first two years of infancy, concentrating in the gray matter and retinal membranes.

In a meta-analysis of 14 trials, DHA supplementation improved visual acuity in a dose dependent manner. In another trial of 341 pregnant women, treatment with cod liver oil from week 18 until 3 months postpartum raised mental processing scores at age 4 years.

This is consistent with observational studies showing positive associations between maternal DHA levels or fish intake during pregnancy and behavioral attention scores, visual recognition, memory, and language comprehension in infancy.

An FDA report issued in 2008 noted that the nutrients in fish – especially n-3 LCFAs, selenium, and vitamin D – could boost a child’s IQ by an estimated ten points. 2

The FDA report summarizes evidence suggesting that the greatest benefits to children would result if pregnant women of childbearing age, nursing mothers and young children ate more than the 12 ounces of fish per week currently recommended by the EPA.

According to the National Fisheries Institute, Americans currently consume only five ounces a week of fish high in n-3 LCFA, which is less than half the recommended amount. The NFI also estimates that up to 14 percent of women of childbearing age eat no fish at all, despite the fact that n-3 LCFA are essential to proper fetal brain and eye development.

Based on the new understanding of selenium’s protective role, and the importance of DHA for fetal and early childhood development, pregnant mothers should be advised to eat oily ocean fish regularly.

Fish consumption and autoimmune and inflammatory disease

The first evidence of the significant role of dietary intake of n-3 LCFA in reducing inflammation came from epidemiological observations of the low incidence of autoimmune and inflammatory disorders in a population of Greenland Eskimos compared with gender- and age-matched groups living in Denmark. The Eskimos in this study had dramatically lower rates of psoriasis, asthma and type 1 diabetes, as well as a complete absence of multiple sclerosis.

Animal and human studies suggest that n-3 LCFA suppresses cell mediated immune responses. Increasing the amount of n-3 LCFA while decreasing omega-6 fatty acids leads to improvements and a decrease of steroid use in patients with rheumatoid arthritis and asthma.

This is because omega-3s have been shown to suppress the capacity of monocytes to synthesize interleukin-1 (IL-1) and tumor necrosis factor (TNF). IL-1 and TNF are the principal mediators of mediation in several different inflammatory and autoimmune conditions.


This is simply a re-cap of the overview presented at the beginning of the article. But it’s worth repeating.
  • Selenium protects against mercury toxicity, and 16 of the 25 highest dietary sources of selenium are ocean fish
  • If a fish contains higher levels of selenium than mercury, it is safe to eat
  • Most species of commonly eaten fish in the U.S. have more selenium than mercury
  • Fish are not significant sources of PCBs and dioxins when compared to meat, dairy or vegetables
  • The benefits of eating fish regularly far outweigh the potential risks, which are neglible
  • Pregnant mothers and young children should eat 2-3 servings of oily ocean fish each week
  1. Energy & Environmental Research Center, University of North Dakota (EERC). EERC Research Finds Mercury Levels in Freshwater and Ocean Fish Not as Harmful as Previously Thought. June 22, 2009. Accessed at http://www.undeerc.org/news/newsitem.aspx?id=343
  2. Energy & Environmental Research Center, University of North Dakota (EERC). EERC Research Finds Mercury Levels in Freshwater and Ocean Fish Not as Harmful as Previously Thought. June 22, 2009. Accessed at http://www.undeerc.org/news/newsitem.aspx?id=343


The gut-skin connection: how altered gut function affects the skin

The gut-skin connection: how altered gut function affects the skin

I’m preparing for my talk at the upcoming Wise Traditions Conference in Santa Clara, CA on November 10th. I’ll speaking on the “gut-brain-skin axis”, a fascinating topic that I’ve been exploring for some time. I hope some of you will be able to come to the conference, but I thought I’d share a little slice of my research here for those of you who can’t. (If you don’t make the conference and want to watch my entire presentation, I believe the Weston A. Price Foundation sells DVDs of the talks after the fact.)

I’ve discussed the gut-brain axis several times on my radio show, and I’ve at least mentioned the triangular connection between the gut, brain and skin. In this post I’d like to go a little deeper on the gut-skin connection. Researchers as far back as 1930 suspected a link between gut and skin health, and modern research has now confirmed the importance of this relationship. And as a clinician who works with people on these conditions, I’d go as far as to say this:
If you want to heal your skin, you have to heal your gut.Tweet This

Associations between gut disorders and skin conditions

Epidemiological evidence shows a clear association between gut problems and skin disorders. A recent report indicated that small intestine bacterial overgrowth (SIBO), a condition involving inappropriate growth of bacteria in the small intestine, is 10 times more prevalent in people with acne rosacea than in healthy controls, and that correction of SIBO in these individuals led to marked clinical improvement. (1) 14% of patients with ulcerative colitis and 24% of patients with Crohn’s disease have skin manifestations. (Interestingly enough, a study just came out showing that a drug normally used to treat psoriasis is also effective for Crohn’s disease.) Celiac disease also has cutaneous manifestations, such as dermatitis herpetiformis, which occurs in 1/4 of celiac sufferers. Celiacs also have increased frequency of oral mucosal lesions, alopecia and vitiligo. (2)

How altered gut function impacts the skin

Intestinal permeability (a.k.a. “leaky gut”) causes both systemic and local inflammation, which in turn contributes to skin disease. In a study way back in 1916, acne patients were more likely to show enhanced reactivity to bacterial strains isolated from stool. 66 percent of the 57 patients with acne in the study showed positive reactivity to stool-isolated bacteria compared to none of the control patients without active skin disease. 1 In a more recent study involving 80 patients, those with acne had higher levels of and reactivity to lipopolysaccharide (LPS) endotoxins in the blood. None of the matched healthy controls reacted to the e. coli LPS, while 65% of the acne patients had a positive reaction. Both of these studies suggest that increased intestinal permeability is an issue for a significant number of acne patients. (4)

Speaking of permeable barriers: most of you have heard of leaky gut by now, but what about “leaky skin”? The main function of the skin is to act as a physical, chemical and antimicrobial defense system. Studies have shown that bothstress and gut inflammation can impair the integrity and protective function of the epidermal barrier. This in turn leads to a decrease in antimicrobial peptides produced in the skin, and an increase in the severity of infection and inflammation in the skin. (5)

The gut flora also influences the skin. Substance P is a neuropeptide produced in the gut, brain and skin that plays a major role in skin conditions. Altered gut microbiota promotes the release of substance P in both the gut and the skin, and probiotics can attenuate this response. (6) The gut microbiota influences lipids and tissue fatty acid profiles, and may influence sebum production as well as the fatty acid composition of the sebum. (7) This may explain why a Russian study found that 54% of acne patients have significant alterations to the gut flora (8), and a Chinese study involving patients with seborrheic dermatitis also noted disruptions in the normal gut flora. 2

Probiotics improve skin conditions

Another line of evidence suggesting a connection between the gut and skin is the observation that probiotics improve skin conditions. Oral probiotics have been shown to decrease lipopolysaccharide, improve intestinal barrier function and reduce inflammation. The first formal case report series on the value of using lactobacilli to treat skin conditions was published in 1961 by a physician named Robert Siver. He followed 300 patients who were given a commercially available probiotic and found that 80 percent of those with acne had some clinical improvement. 3 In a more recent Italian study involving 40 patients, Lactobacillus acidophilus and Bifidobacterium bifidum in addition to standard care led to better clinical outcomes than standard care alone. (9) And another recent study of 56 patients with acne showed that the consumption of a Lactobacillus fermented dairy beverage improved clinical aspects of acne over a 12-week period. (10)

The beneficial effect of probioitics on skin may explain why pasteurized, unfermented dairy is associated with acne, but fermented dairy is not. I haven’t seen any studies on raw dairy and skin conditions, but my guess is that it wouldn’t be associated either. Orally consumed probiotics reduce systemic markers of inflammation and oxidative stress, both of which are elevated locally in those with acne. (11) Oral probiotics can also regulate the release of pro-inflammatory cytokines within the skin. (12) The fermentation of dairy reduces levels of insulin-like growth factor 1 (IGF-1) by more than four-fold. (13) This is significant because studies show that acne is driven by IGF-1, and IGF-1 can be absorbed across colonic tissue. (14) This would be particularly problematic when increased intestinal permeability is present, which as I mentioned above is often the case in people with acne.

Now I’d like to hear from you. Have you noticed a connection between gut health and skin conditions in your own experience? Has healing your gut improved your skin? Let us know in the comments section.
  1. Strickler A, Kolmer JA, Schamberg JF: Complement fixation in acne vulgaris. J Cutaneous Dis 1916, 34:166-78.
  2. Zhang H, Yu L, Yi M, Li K: Quantitative studies on normal flora of seborrhoeic dermatitis. Chin J Dermatol 1999, 32:399-400.
  3. Siver RH: Lactobacillus for the control of acne. J Med Soc New Jersey 1961, 59:52-53.


You're a Vegetarian. Have You Lost Your Mind? | Psychology Today

You're a Vegetarian. Have You Lost Your Mind? | Psychology Today

Vegetarian diets are correlated with an increase in mental health problems

Entirely vegan diets are unknown among traditional human cultures. Back in the early part of the 19th century, dentist and explorer Weston Price went looking for vegans, but found only cannibals*. Since vegan diets in nature provide no vitamin B12 and very little in the way of usable long chain omega3 fatty acids, it is not surprising that humans have continued to eat animals and animal-derived products. Nowadays one can obtain algae-derived DHA (the major long chain omega3 fatty acid present in the brain). and supplement B12. That wasn’t possible until a few years ago, and there’s little evidence that supplementation with DHA alone is helpful for the brain.

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We have been encouraged to eat more plants and less animals. Various writers have suggested it is healthier for our bodies and our planet. I have no objections to a mostly plant-based diet as long as attention is paid to protein requirements and micronutrition. However, since little things in animal products (some essential like B12, some that can be created in our bodies but perhaps not in the amounts we need, such as creatine) seem to be very important for the brain, it’s interesting to look at the literature on vegetarian diets and mental health. Here is the latest (and the best) observational study:  Vegetarian diet and mental disorders: results from a representative community survey.

It's a German study, and for a large population-based retrospective observational design, it's actually fairly thorough and sensible.  And if you are a vegetarian, it certainly doesn't say that vegetarianism causes mental health problems.  But in all but two studies done in the past, vegetarianism has been linked with higher rates of depression, anxiety, and particularly eating disorders (bingeing, restricting, and purging behaviors).  But to be perfectly honest, all those studies had some serious limitations (they were small, done special populations, and often measures based on just a few answers to general survey questions).  I've reviewed a few of them.  (My favorite has to be the one where they calculated arachidonic acid ingested to the hundredth of a gram based on data from a food frequency questionnaire, which seems very unlikely to be accurate)  I don't think it is a coincidence that the two positive studies were done by the same group of researchers in the Seventh Day Adventist population.

The interesting thing about the general trend that vegetarians aren't quite as mentally healthy as omnivores (in observational studies) is that vegetarians tend to do better in other measures of health. They are better educated, as a population they are generally younger, less likely to smoke or drink, more likely to exercise, and they tend to care about ethics and the quality of their food. However, vegetarians are also more likely to be female (which is more likely to be associated with anxiety, depression, and eating disorders by a long shot).

So this new study has some things to recommend it. For one thing, the mental health diagnoses were determined not by answers to typical questionnaires, but by a full clinical interview using psychologists or physicians, lasting an average of 65 minutes each. (Pretty impressive, considering there were over 4,000 participants in the population-based study). In addition, the researchers matched omnivores to vegetarians based on age, education, sex, and whether they were urban or rural and crunched those numbers as well, so we got a good sample that took out some of the major confounders that dogged the previous studies. Finally, this cohort was a purposeful random sampling of the German adult population (excluding people over 65, however), rather than the Seventh Day Adventists or adolescents and college students sampled in previous studies.

And when the researchers went down the line of depressive disorders, anxiety disorders, somatoform disorders (things like body dysmorphic disorder, health anxiety and hypochondriasis), and eating disorders, the mostly vegetarian were more likely to be afflicted, and the strict vegetarian even more likely.** The full blown eating disorder diagnoses were rare enough, however, that the researchers didn't compute the odds ratios, as they felt the dataset was not robust enough to be fair. Compared to the general population, the vegetarians were more likely to have mental disorders, and compared to the sex and education and population and age matched controls, the risk of mental disorders in vegetarians really shot up, with odds ratios hovering around 2 fold increased risk, some as high as 3 fold.

When the data was taken apart from another direction, it was found that participants in the study with depressive, anxiety, somatoform, and anxiety disorders consumed less meat than people without a mental disorder. The amount of vegetables, fruits, fish, and fast food did not have a consistent pattern separating those with and without mental disorders (except fish consumption was linked with reduced anxiety. Hmmm).  In fact, unlike the 2010 Australian study, those with mental disorders in this German population were less likely to consume fast food than the mentally healthy population.

Temporally, the adoption of a vegetarian diet, on average, tended to follow the mental health diagnosis, suggesting that the vegetarian diet was not in fact causal. I know originally the abstract of the article said the opposite, but if you read the full text, you find that the abstract was misrepresentative. A retrospective study isn't the most robust way to determine this issue, but I would tend to believe this timing to be true, particularly for anxiety disorders, which often begin before the age of 10. The main exception to the temporal findings in this study were the eating disorders, which tended to start right around the same time as adoption of a vegetarian diet. As I've reported before, several of my eating disordered patients have told me they adopted vegetarianism so they would have an excuse to restrict food and not have to eat in public.

So what is going on? In Germany, are the neurotic perfectionists who are more likely to be choosey about food (and thus select vegetarianism and eschew fast food) also more vulnerable to depression and anxiety? Sure, could be. Or maybe those with mental troubles try to avoid what is thought to be bad food (meat and fast food). It is also possible that the nutrient deficiencies common in vegetarian diets (the most robustly studied being long chain omega 3 fatty acids and B12, though I think zinc and creatine and even too low a cholesterol could also be issues) could accelerate or worsen pre-existing mental conditions.

A large study comparing choosey, neurotic, perfectionistic omnivores (ahem) with strict vegetarians would be interesting, I think.

*these cannibals preferentially ate fisherman, who would be chock ful of long chain omega3 fatty acids!!

**the German word for "meat" excludes poultry.
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Copyright Emily Deans, MD