An audio version of this post is available here.
I previously discussed the obesity causation topic a bit in the Weight Gain and Obesity chapter of ETFOH. However, I didn’t go too in-depth and didn’t sufficiently connect it causally with vitamin A. I’ll now try to more solidly establish that connection here.
When I first started on my vitamin A elimination diet one of the very unexpected side-effects was the effortless weight loss. My experience was not a one-off either. I had a (non-diseased) colleague report the same result. Even though we had vastly simplified our diets, it was still providing ample calories (3,000 or more) and all the required nutritional elements. Although n=2 in this study, for two men in their late fifties, to quickly drop around 30 pounds each, and without trying at all to do so, that result was quite intriguing. There was indeed something very unexpected going on here. It’s especially so considering that we’ve both effortlessly kept that weight off for three years now too.
So, with that experience, I had theorized that the body was simply getting rid of fat it no longer needed. More specifically, I had theorized that the body had originally stored the additional fat as a protective measure against excess circulating retinol. Basically, the adipose tissues were taking on some of the load from the liver and thereby scrubbing excess retinol out of circulation. After all, for the liver to take on more retinol storage, it absolutely must get fatter to accomplish that task.
But, at the same time, I was not very satisfied with that simplistic explanation for the adipose cells either. The problem with it was: why were these adipose cells that were taking on the extra retinol not themselves adversely affected by it too? Why don’t they become inflamed and invoke an auto-immune reaction as do the stem cells of the epithelium’s? Well, it took a while for me to see the obvious. Quite obviously, they are indeed being affected in almost the same way. The important distinction is that the adipose stem cells are much simpler in structure and don’t generate the complex cell adhesion proteins needed to tightly stitch themselves to each other. Since they don’t generate these proteins, then they don’t generate the immune-alerting defective and foreign‑species looking proteins. But, the way that the adipose stem cells do behave similarly to the epithelium stem cells in response to vitamin A toxicity is that they too are forced into a perverse state of abnormal rapid replication. At least that was my sub-theory on the causal mechanism.
Of course, many people will quickly conclude that it was the sugar reduction that was responsible for the fat loss my colleague and I experienced. However, that’s simply not true. I tested that possibility by consuming quite a lot of sugar, and the weight did not come back. I also used the following charts in ETFOH to demonstrate the sugar alone is not to blame for the original weight gain. Here’s a copy of that section for easy reference.
Let’s consider the obesity trends that are going on in the USA, Canada, the UK, and chocolate-loving Switzerland. This trend pattern is quite revealing.
Figure 1 Average Daily Sugar Consumption for Selected Countries
There are a few very important observations to make here. The first is to note that Switzerland’s average daily sugar consumption is higher than that of Canada’s, and has been consistently so for about the last five decades. The second observation is the significant and steady decline in consumption of sugar in the UK. Next, let’s look at the trend lines for obesity in these countries.
Figure 2 Average BMI for Selected Countries
Even though Switzerland has higher average daily sugar consumption than that of Canada, they have significantly less obesity. More striking is the slope of the trend lines. Canada’s trend is dramatically higher. Next, consider the contradiction in the sugar consumption between the UK, and Canada. Even though the consumption in the UK has steadily dropped significantly over this time, and Canada’s has steadily increased over this same time, the average BMI trend lines for these two countries are nearly identical. Therefore, this completely contradicts the theory that sugar consumption is causing obesity. Additionally, many other people who do eliminate sugar from their diets do not experience much weight loss, and if they do, they can’t seem to keep it off.
Then whenever I traveled to the USA, I noticed that there is a significantly higher rate of obesity, and even moderately overweight people there than compared to Canada. This is no small detail. Statistically, about 70% of all Americans over the age of 20 are now overweight or obese. (https://www.cdc.gov/nchs/fastats/obesity-overweight.htm).
But, you don’t have to look a statistical data; it is easy to see it almost everywhere you go. Just walk down a busy street, or go to a supermarket and scan the crowd. Just making a rough ballpark type guess, I’d put the USA at having about 30% more serious obesity than compared to Canada. How can that be possible? Both the USA and Canada have our dairy supply “supplemented” with vitamin A so that alone can’t account for the difference. But, it’s quite understandable when you learn that many of the breads, flours, and breakfast cereals in the USA are “supplemented” with vitamin A whereas in Canada they are typically not.
Some people might want to interject here and blame the differences in our national obesity rates just on lifestyle choices. But, that excuse does not cut it either because the lifestyle in the USA is very similar to that of Canadians too.
Then when I traveled in Mexico, the obesity epidemic there appeared to be even worse than that of the USA. There are a lot of poor people in Mexico who are clearly not living the high-life or sedentary lifestyles and are yet quite obese. What’s going on there? Doing just a trivial amount of investigation, this rate of obesity is completely and totally abnormal for the Mexican people too. Sure, there’s a lot more sugar being consumed in Mexico nowadays, but we know that sugar alone can’t be blamed. So then, what’s really going on? Well, when I learned that sugar in South America was being “supplemented” with vitamin A, it became rather clear. When I was in Mexico I went to a supermarket, picked up a pack of sugar, read the nutrition label, and sure enough pure table sugar was labeled to provide 10% RDA of vitamin A. That’s correct, some of their sugar is laced with vitamin A. Then when you see just how much soda is consumed in Mexico, and that vitamin A supplemented sugar is likely in their soda also, we have a prime suspect.
Next, let’s now get back to what’s happening in the USA and consider some supporting scientific evidence to make the case against vitamin A. Firstly, let’s look for some correlations.
Figure 3 Serum Retinol level and BMI in USA
Source: Serum retinol distributions in residents of the United States: third National Health and Nutrition Examination Survey, 1988–19941,2 Carol Ballew, Barbara A Bowman, Anne L Sowell, and Cathleen Gillespie
Isn’t that a remarkable correlation? As we get older, not only do our serum retinol levels creep up but so too does our BMI levels. Except, it’s not just the BMI levels that creep up with age, it’s also our incidence rates of the auto-immune diseases and cancers. Of course, as our obesity rates climb our life expectancy rates correspondingly decline. So, that drop off in BMI for the 80-90-year-olds shown in the chart is not because they are finally getting their weight under control. Rather, it’s because the more obese folks have died early and have thus statistically diluted the numbers.
Additionally, isn’t it peculiar that for young kids (when they have low vitamin A serum levels) they typically have tons of energy, nice thick hair, nice smooth skin, good vision, low cholesterol levels, and a normal BMI? Unfortunately, as we get older, we typically start to lose these indicators of good health. Next, let’s consider the vitamin A – BMI correlation in South Korea and see how it compares to that of the USA.
Figure 4 Serum Retinol level and BMI in the USA and South Korea
Source: Nutrition Research and Practice (Nutr Res Pract) 2012;6(1):45-50
pISSN 1976-1457 eISSN 2005-6168
Vitamin A status of 20- to 59-year-old adults living in Seoul and the metropolitan area, Korea. Sungah Kim, Young-Nam Kim and Youn-Ok Cho
The average South Korean vitamin A serum levels of vitamin A are much lower than that of Americans of the same age. Correspondingly, so are their BMI levels. Maybe even more important is that the average BMI levels in South Korea are rather steady over a wide age range and only creep up slightly by age 60. So, it could be that serum levels above 1.5 µmol/L are dangerous, whereas those below are more safely manageable by the body’s regular defense mechanisms.
Of course, we all know that correlation alone does not determine causation. In the field of causation theory there is a fundamental premise that states that causation cannot be inferred without manipulation. What that means is that to claim a causal influence we need to prove that directly manipulating an input variable has a corresponding measured response (within some range of statistical significance).
Fortunately, we do indeed have that supporting evidence to claim a causal factor with the retinoids and obesity. Firstly, we have the somewhat inadvertent results from a study where dietary vitamin A (even in the form of beta-carotene) was increased resulting in obesity. I say inadvertent results, because neither the researchers, nor the subjects, were at all interested in, or even suspecting, to see a resulting change in body weight.
Source: Vitamin A and vitamin E in human blood 3
Levels in patients in psychiatric hospitals
BY 2. A. LEITNER
52 Welbeck Street, London, W I AND T. MOORE AND I. M. SHARMAN
Dunn Nutritional Laboratory, University of Cambridge and Medical Research Council
This study is from 1951 -1962, the researches were working with patients in a UK psychiatric hospital, often including people with schizophrenia. What they noticed is that the serum levels of both vitamin A and the carotenoids in these patients was abnormally low. Somewhat surprising to me, the researchers did not appear to think that there may have been a possible connection between the patient’s mental health condition and their vitamin A status. Nonetheless, the researchers felt that it would just be in the best interests of the patient’s overall general health to bring their serum levels in line with what was deemed to be the more normal values as observed in the general public. With that, they added some higher concentration beta-carotene vegetables into the meal plan for the patients. The very surprising outcome of that diet manipulation was that many of the patients quite quickly became obese.
Our results have shown not only that mean values for carotenoids, and usually also for vitamin A, are low in mental patients, but that values approaching those for normal subjects may be induced by ensuring that large amounts of carotene are consumed, either in oily solution or in the form of vegetables.
Somewhat lower values were always found, for both carotenoids and vitamin A, in patients who had been resident in hospital for 2 years than in newly admitted patients. In certain groups of newly admitted patients the vitamin A levels were normal, but the carotenoid levels were always low.
Between the two stages of our work, begun in 1951 and in 1962, special attention has been given at Claybury Hospital to the provision of liberal supplies of vegetables. As in most other psychiatric hospitals, moreover, the use of tranquillizing drugs has improved the appetites of the patients, to such an extent that obesity has become a common problem. At the most these changes seemed to have caused only a slight increase in blood levels of carotenoids and vitamin A towards the normal range.
Yes, adding more vegetables, such as carrots to the diet (and the tranquilizing drugs) led to obesity. And then regarding the tranquilizing drugs being to blame for the improved appetites, they contradict themselves with the following rationalization statement:
A likely hypothesis is that the appetite of mental patients for vegetables is poor, and that these are not eaten in amounts typical of normal subjects unless special measures are taken.
An alternative hypothesis, perhaps less probable, is that in mental patients the efficiency of the absorption and conversion of carotene is reduced. Increased quantities of carotene must therefore be given, above the requirements of normal subjects, in order to sustain levels of carotenoids and vitamin A equal to those in normal subjects.
Source: as above
Regardless, I like these types of inadvertent experiments because they are ideal double-blind studies. Neither the researchers nor the people in the studies realized or were even aware that the effect on obesity was being considered as an outcome. As a side note, many people with schizophrenia report a surge in weight gain just before their first encounter with the disease conditions. Also, very interestingly, the lower than normal level serum levels of vitamin A is observed in autism, IBD, depression, and Alzheimer’s disease too. Most surprisingly, it’s very significantly so in cystic fibrosis too. So, where is their serum retinol magically disappearing too? Could it be into retinoic acid? Isn’t it also interesting that the documented psychiatric side-effects of retinoic acid toxicity are a perfect match for the symptoms of schizophrenia, autism, and even Alzheimer’s? I digress. Let’s get back on track with investigating obesity causation.
Next, we have the opposite effect demonstrated in another study where the vitamin A input variable is manipulated in the other direction.
Proc Nutr Soc. 1973 Dec;32(3):105A-106A.
Vitamin-A and epilepsy: a dietary contretemps.
Sharman IM, Stern G.
In this 1973 study researchers were considering the possible effect a low vitamin A diet may have had on epilepsy. Very surprisingly, and completely unexpectedly too, what they saw was a rapid loss in body fat. The study was terminated because they believed that the rapid drop in weight in their subjects was a sign of vitamin A deficiency.
And then in another experiment attempting to purposely induce vitamin A deficiency in volunteer adults we have:
From the sample menus he provided, one can estimate that on a typical day, a subject [person] would consume 80–160 IU of carotene. Thiamin was estimated to be adequate and ascorbic acid was given as a supplement. Energy density was kept high, to prevent weight loss due to lack of appetite and “for psychological reasons.” Indeed, for the first 3.5 mo, all subjects [persons] gained weight. After that time, for the following 2.5 mo, all 10 people simultaneously lost amazingly large amounts of weight, e.g., two persons lost 10 kg of their maximal weights (79 kg and 59 kg). The author interprets this weight loss to be a consequence of the exhaustion of the subjects’ vitamin A reserves, and compares it to the weight loss observable in vitamin A–deficient rats.
Source: The Experimental Induction of Vitamin A Deficiency in Humans
George Wolf Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720-3104
By combining the results of these three studies, we’ve satisfied one of the key requirements of making a causal association claim. Therefore, we have both a solid correlation and required manipulation experiments supporting our general theory. But, what about that specific sub-theory that retinol overload is driving adipose stem cells into an abnormal state of more rapid replication? Surely this has been investigated. After all, the retinoids and more specifically vitamin A, and retinoic acid are some of the most studied molecules in all of medical science. It has indeed been studied. Here’s a 2016 report documenting the adipose genesis effect of retinoic acid: Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome
Adipogenesis is a differentiation process regulated by the complex interaction of some RXR heterodimeric partners (18). In 3T3-L1 adipocyte differentiation assays, retinoic acid effects vary as a function of the stage of adipogenesis and relative retinoic acid receptor, peroxisome proliferator-activated receptor-γ, and RXR expression (19). Inhibition of endogenous RA production by the inactivation of retinaldehyde dehydrogenase (the primary retinaldehyde metabolizing enzyme) increased energy dissipation and reduced abdominal fat accumulation, thus preventing and ameliorating diet-induced obesity (20). Although the role of RA in adipogenesis has been generally proven in vitro, little information on the relationship between serum RA level and MetS (as well as its components) is available for the Chinese population..
Source: Yan Liu, Hongen Chen, Di Mu, Jiahua Fan, Jiayi Song, Yuan Zhong, Di Li, Min Xia; Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 4, 1 April 2016, Pages 1686–1692, https://doi.org/10.1210/jc.2015-4038
Even though the documented adipose genesis is being induced by retinoic acid, we need to remember that retinoic acid is readily produced just by a somewhat high dietary intake of vitamin A.
Retinoic acid is present in both the fasting and postprandial circulations where it is bound to albumin. Immediately following consumption of a retinol-rich meal (~1 mg/kg body weight), mean plasma concentration of retinoic acid was observed to reach 254 nmol/L but was quickly restored to fasting concentrations of 14 nmol/L in 10 male volunteers (Arnhold et al., 1996).
DRAFT SCIENTIFIC OPINION 1
Scientific Opinion on Dietary Reference Values for vitamin A1 2
EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA)2, 3 3
European Food Safety Authority (EFSA), Parma, Italy
The oxidization of retinol into retinoic acid will happen even more so once a person ages and starts approaching their liver’s maximum storage capacity. But, let’s not forget that in North America, much of our dairy is being directly supplemented with additional retinol too.
Vitamins A and/or D should be considered in the hazard analysis for plants fortifying milk products, as over-fortification could result in toxic levels (). The target level for vitamins A and D in milk manufactured in the US is 2000 IU/quart and 400 IU/quart, respectively. The US-FDA currently considers levels in excess of 6000 IU/quart vitamin A and 800 IU/quart vitamin D to be potential health concerns (Nichols, 1992). Vitamin fortification might be controlled under a CCP or a PP, depending on a firm’s hazard analysis. Preventing over-fortification is accomplished by careful monitoring of vitamin concentrate addition, proper measurement of pump feed rates, and determining whether the volume of concentrate used per product batch is in relative agreement with the theoretical value required to achieve the desired fortification level.
Source: Hazard Analysis Critical Control Point and other food safety systems in milk processing
S.C. Murphy, in Improving the Safety and Quality of Milk: Milk Production and Processing, 2010
Therefore, the chances of surging one’s retinol intake are considerably higher with frequent milk and cheese consumption. And, yes, there has been a case in Canada where a dairy producer did not have the injection pumps set correctly, and some kids were subsequently killed by drinking the milk. Somewhat strangely, even though fortifying low-fat milk is a legislated requirement in Canada and the USA, it’s not in the UK. How can it be that all those people in the UK drinking low-fat dairy have managed to avoid vitamin A deficiency symptoms? Sorry, I digress again.
Pasteurized Milk Causes Scurvy
What about pasteurization? Could the heating of casein with its embedded retinol generate retinoic acid too? I think it probably does. Here’s why. Firstly, consider this report:
The Effect of Holder Pasteurization on Nutrients and Biologically-Active Components in Donor Human Milk: A Review
From Table 4. Cont. on Page 10
A 34% reduction in vitamin A is reported after pasteurization, and categorized as being “significant.”
Okay, so what happened to the missing retinol post pasteurization? Where did it disappear to? Of course, it didn’t just disappear. It was oxidized and otherwise broken down. Then consider this interesting little ditty? Pasteurized milk is reported to cause “scurvy” too.
Most people are familiar with scurvy, a disease that results from vitamin‑C deficiency. Fortunately, scurvy is rare in Western societies. (It is still seen in infants who are fed a diet of boiled or pasteurized milk). Osteoporosis can be caused by vitamin C deficiency and is seen in both infants and adults who have scurvy. Vitamin C is important in the production of a material called collagen. Collagen is perhaps best described as a fibrous tissue into which mineral is deposited in bone. Together with mineral, collagen gives bone its strength. While it is clear that vitamin C is necessary for bone health, vitamin C deficiency is rare. Vitamin C supplementation as a general preventative measure for osteoporosis does not appear to be warranted. […]
Vitamin A is also popularly known today as beta-carotene. Beta-carotene is actually a precursor to vitamin A. Vitamin A is considered critical to normal growth of the skeleton, but excessive vitamin A poses real dangers. Vitamin intoxication causes weakness, fatigue, emotional disturbances, headache, aching in the muscles and bones. Unfortunately, vitamin A is also one of the vitamins often taken in excess in the United States because of recent reports suggesting its beta-carotene content may protect against cancer.
Source: The Osteoporosis Handbook
Sydney Lou Bonnick
Taylor Trade Publishing, Oct. 1, 2000 – Health & Fitness
How can it be possible that for infants drinking pasteurized or boiled milk instead of raw milk there’s an increased risk for scurvy? That does not appear to be logical because milk, pasteurized or not, contains only trace amounts of vitamin C at ~0 mg/100 g. But then consider the 1937 study, titled:
CONCERNING THE TOXICITY OF VITAMIN A
EDWABD B. VEDDEB AND CHABLES BOSENBEBG
Department of Experimental Medicine, George Washington University
Medical School (Received for publication December 17, 1937)
In this study, the researchers believed that they had induced “scurvy” in their animals just by having them on high vitamin A diets.
Since the rat is known to be capable of synthesizing vitamin C and is not susceptible to scurvy, it is difficult to explain this action of vitamin C. A possible explanation is that vitamin C destroys the toxic factor and that all the vitamin C synthesized by the rat is used up in this process, leaving it susceptible to scurvy. Scurvy of the rat has never been described, but the symptoms produced by fish liver oils are not unlike scurvy; they include failure to grow, hemorrhages, particularly from the eyes and nose but to some extent from other mucous membranes, and abnormal rarefaction and fragility of the bones.
In a few rats, the urine was collected and titrated with 2,6-dichlorophenol indophenol. After administration of jewfish liver oil equivalent to 100,000 units of vitamin A for about 3 weeks, the excretion of vitamin C decreased to the vanishing point, but reappeared in the urine in considerable amounts after the daily administration of 5 mg. of crystalline ascorbic acid. While this is suggestive, since the physiological action of vitamin C is quite unknown, the correct explanation of its remedial action for jewfish liver oil must await further experimentation.
So, even though rats can produce their own vitamin C, that wasn’t enough to protect them. Whereas the added vitamin C in these experiments was rather effective in protecting the animals from dying due to the toxicity effects of the vitamin A. Of course, there’s more to it. These researchers knew it was not just simply vitamin A alone causing the disease conditions. They make this very interesting and astute statement in their conclusion:
In addition to vitamin A, fish liver oils contain a toxic principle, at present not identified.
Since retinoic acid was discovered around 1960, these researchers back in 1937 would not have known about it as being the hidden additional toxic principle that was causing the “scurvy” in addition to all the other diseases and ultimate death in their animals.
Next, consider this little ditty from the same study:
When the unitage of vitamin D exceeded that of vitamin A, the combination was far more toxic than the same amount of vitamin A alone.
Of course, many people in North America have been consuming fish oils thinking that it is good for us. And then remember that those injection pumps at the dairy producers are pumping both vitamin A and D directly into our low-fat milk supply. Therefore, in North America, there is no shortage of possibilities for people to be getting too much retinol in their daily diet. Of course, it’s not just retinol, as reported above. It is also quite normal to have trace (nmol) amounts of retinoic acid in serum too. Those facts combined with the 2016 report documenting that retinoic acid induces adipose genesis, that eliminates the theoretical aspect of our sub-theory. Therefore, very slowly, over the years, vitamin A and daily spikes in its downstream metabolite of retinoic acid are just going to make us fatter and fatter.
So, with this final detail established, we now have solid supporting correlations, manipulation experiments, and a direct documented causal mechanism. That should leave you with so little doubt as to one of the major forces driving the obesity epidemic. That’s all rather bad news. But, the good news is that our intake of retinol is under our control, and obesity caused by it is quite readily reversible too. I am now getting direct reports from people who are dropping amazing amounts of weight after adopting a vitamin A-free diet. Here are just a few examples:
I have been losing a lot of weight – 50 pounds in the last 15 weeks – and expect to lose another 40 pounds in the months ahead.
In 6 months, I lost 80 Lbs and my Skin Cleared up.
After four months of being on a vitamin A elimination diet I’ve lost thirty pounds. It has just evaporated.
Even though I’m now consuming about 5,000 calories per day, I’m not gaining weight.
Nonetheless, I don’t want to put the entire blame for obesity on vitamin A either. Like with so many other aspects of the autoimmune diseases and the psychiatric disorders, there is no single cause. The root-causes and mechanisms are more complicated and multi-factored. For example, let’s consider the combined effects of retinoic acid and sugar. As that retinoic acid drives up the rate of adipose genesis, those new cells will in turn demand more energy. That then drives up the appetite and the craving for sugar or other sources of glucose. It’s all very subtlely and yet directly interconnected. I’m also quite sure that there are vitamin A free diets that could still induce the obesity effect if regularly over-consumed. But, at least you now know the identity of one of the most significant hidden factors. It’s a poison “vitamin” that’s making many of us fat and sick.