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“Triple-Fat-Gainers”: Extra Health Hazards

“Triple-Fat-Gainers”: Extra Health Hazards
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  • Significantly greater risks of cognitive decline, cancer, low testosterone, high cholesterol, high blood pressure
  • The same diet and exercise program reduces all of these extra risks

Did you know that some of us put on three times more fat while eating exactly, precisely (repetition intended!) the types and quantities of foods as others? Did you know that these “triple-fat-gainers” will ultimately be diagnosed with type 2 diabetes? And that the same body chemistry—uncorrected—significantly increases risk of dementia, cancer, cardiovascular disease, loss of vision, and kidney failure? And that’s not all!
The term “triple fat gainer” is literally descriptive of the outcome of one of many “sugar research” studies done by Prof. John Yudkin, MD, PhD of Queen Elizabeth College in London. My reading this study and his 1972 book about sugar—Pure White and Deadly—just before opening the Tahoma Clinic in 1973 has guided my approach to prevention and treatment of type 2 diabetes ever since.
“Triple-fat-gainer” is my term describing the average nine pounds gained by university students with a family history of type 2 diabetes as compared with the average three pounds gained by other university students with no family history of type 2 diabetes in just one month, while both groups were eating exactly the same high-sugar diet! Yes, that’s nine pounds as compared with three pounds: triple-fat-gainers!
The body chemistry which causes this triple fat gain is unfortunately shared by 115 million[i] of us in these United States. As the population of our country is 318.9 million[ii] (both figures from 2014), that’s 36% of us!
How can it be that a little over one in three are triple-fat-gainers? Have chemicals in food, food refining, water pollution, air pollution, cell phone towers, chemtrails, lack of exercise, and all the other hazards of “modern” civilization caused it? Many of these problems can aggravate and accelerate this situation, but aren’t the actual cause.
The cause is hundreds of thousands of years old! Way back then, having the body chemistry of a triple-fat-gainer was actually an advantage! And it wasn’t accompanied by higher risks of all the diseases listed above. Why was triple-fat-gaining body chemistry an advantage—good for us!—hundreds of thousands of years ago, and actually continued to be good for us until the “invention” of farming, which (depending on which researchers we’re reading) was “only” 9,000 to 11,000 years ago?
Before farming, humans living in the northern and southern hemispheres ate what they could find—small animals, large animals, fish, various roots, leaves….where’s the “carb” in that? Yes, fruits, berries and mushrooms appeared “in season,” but except in the tropics, there wasn’t a gatherable supply of relatively high carbohydrate foods year-round.
What do foods higher in carbohydrate do in our bodies? When digested and absorbed, higher carbohydrate foods raise blood sugar (glucose), which in turn signals the pancreas to make more insulin. Insulin’s job is to help transport the glucose into nearly every cell in our bodies, where it is “burned” for energy, and any excess is stored as fat.
No one yet knows when, where or how, but back in the “mists of prehistoric times” when hunting, fishing and gathering were the only ways to eat, some (but definitely not all) peoples’ insulin secretion response to eating carbohydrates changed dramatically. As compared with everyone else, these individuals’ pancreatic islet cells would make twice, three times or more the amount of insulin in response to eating carbohydrates.
When more insulin was secreted, more sugar was transferred into nearly every cell in their bodies. The larger amount of sugar couldn’t be “burned” all at once for energy, so more of that sugar was stored as fat, and—there we have it—these individuals are the “remote ancestors” of our modern-day “triple-fat-gainers”, and at that time, being a “triple-fat-gainer” was an advantage, very specifically a survival advantage for the “hunter-gatherer” humans living in the Northern and Southern hemispheres of our planet.
In those areas, higher carb foods—fruits and berries—were available only at specific times of years, mostly later in the summer and into early fall.
When individuals possessing the “triple-fat-gainer” pattern of insulin secretion ate those seasonal berries and fruits, they put on three times as much fat as individuals by the time winter arrived as did individuals with the “regular” insulin secretion pattern.
When cold and relatively cold winters arrived and food was scarce and sometimes very scarce, the “triple-fat-gainers” were of course fatter, and more likely to survive until springtime—and have children—than individuals with the regular insulin secretion and lower fat storage pattern, who just might not make it through a colder, scarcer food winter. Even after farming arrived, there were still “feast and famine” times; among other places, they’re mentioned more than once in the Bible. “Triple-fat-gainers” would be more likely to survive famines, too.
So the “triple-fat-gainers” insulin secretion pattern was a survival advantage for most of human history. Why has it “morphed” into such a disease-causer in just the last century or two?
The problem is that extra-high insulin signal evoked by carbs. If it’s unusually high for those few weeks a year when hunter-gatherer people are “chowing down” on berries and fruits (almost forgot the occasional victory over bees resulting in extra honey consumption!) but not higher the rest of the year when there’s very little carb stimulus, human bodies can handle that. But in “modern times” when sugar, high-fructose corn syrup, and many other varieties of carbohydrate are available “24/7,” our bodies start to ignore that high insulin signal. Technically, that’s called “insulin resistance.”
Think of it this way: when your Dad or Mom yelled at you from time to time when you were a child, you listened and likely did as you were told. But if your Mom (or more likely Dad) yelled at you all the time, you “tuned out.” The longer the yelling went on, the less you responded. It’s the same with our bodies’ response to high insulin—if it’s not present very often, not a problem, if present all the time, our bodies try to tune out.
But what would happen if the insulin couldn’t get the blood sugar into the cells? We’d rapidly run out of energy to burn for nearly every bodily process! So when our bodies try to ignore the high insulin signal by developing “insulin resistance,” our pancreas islet cells make an ever-increasing amount of insulin to keep putting the same amount of sugar into the cells.
The unrelenting pressure of carbohydrates “every day, every day” causes a decades-long upward spiral of “more insulin, more insulin resistance, even more insulin, even more insulin resistance, even more insulin than that, even more insulin resistance than that, and ever-upward” which culminates with insulin resistance so “tough” that even the by-now-extremely high insulin signal can’t get as much sugar as before out of the blood into the cells. So there’s progressively more sugar in the blood, and when that’s detected it’s “officially” diagnosed as type 2 diabetes: high blood sugar and high insulin! (For the record, type 1 diabetes is high blood sugar and very low or no insulin.)
This situation is completely correctable without any patent medications at all! (More about that later.) For now, let’s briefly review four of the many troubles caused by that decades-long upward spiral of insulin.


We’ll start with a quote from a research review:[iii]
Insulin is a master regulator of…..aging in all known species, determining the rate and expression of aging in multiple body systems. Thus, it is not surprising that insulin also plays an important role in brain aging and cognitive decline that is associated with pathological brain aging….Brain insulin resistance may be associated with neurodegenerative diseases such as Alzheimer’s disease, and the condition which precedes Alzheimer’s disease, known as “amnestic mild cognitive impairment.
With 115 million Americans either pre-diabetic (insulin signal spiraling ever-upward) or already diagnosed with 2 diabetes, it’s no wonder that cognitive impairment and Alzheimer’s disease are affecting more and more millions!


Leptin is a hormone made by fat cells; more fat cells, more leptin. Higher insulin levels (which occur in ever-greater amounts for decades before the actual diagnosis of type 2 diabetes) increase leptin production; higher levels of cortisol (the well-known stress-response hormone) also increase leptin[iv]. “Triple-fat-gainers” (who ultimately become type 2 diabetics) of course have more leptin than others.
Research using prostate cancer cells found that leptin decreased the response of the estrogen receptors designated as “beta” receptors (ERb), which are known to be “anti-carcinogenic” receptors.[v] In experimental animals, stimulation of ERb with the anti-carcinogenic testosterone metabolite 5a-androstane-3b,17b-diol (“3b-Adiol”), causes regression of prostate cancer and counteracts metastasis (remote spread).[vi]
So even if a man’s levels of “3b-Adiol” are adequate, the more leptin he has, the less well 3b-Adiol can help his prostate fight cancer.
In addition to “stealing” some of the anti-carcinogenic effect of ERb, leptin also increases the activity of the pro-carcinogenic estrogen receptor alpha (Era). It’s a “double whammy”: leptin increases pro-cancer activity and decreases the anti-cancer activity of estrogen receptors, for both men and women!
We’re not done with the cancer-promoting effects of leptin. Leptin increases levels of another pro-carcinogenic estrogen, 4-hydroxyestrone, and decreases levels of the anti-carcinogenic estrogen 2-hydroxyestrone as well as levels of the exceptionally potent anti-carcinogenic estrogen 2-methoxyestradiol. (2-methoxyestradiol is so potent that patent medicine companies are frantically scrambling to make an unnatural but patentable “derivative” of it!.)
Once again, leptin is decreasing “good” estrogen and increasing the “bad” version of estrogen, giving both men and women higher risk of cancer.
Remember: Excess insulin = more fat = more leptin = higher cancer risk.
One more note: in postmenopausal women, “metabolic syndrome” (which is caused by a decades-long overly high insulin signal, see above and below) is associated with more aggressive breast cancers.[vii]


This one’s so well known to research scientists that I’m not bothering with any footnotes. (Shouldn’t more than one footnote be called feetnote? But back to the real topic….)
In both men and women, testosterone is transformed into estrogen by an enzyme called “aromatase.” By Nature, women’s bodies transform testosterone into estrogen very efficiently, leaving only a little testosterone behind. Men are much less efficient at (among other things, just ask many women about male efficiency!) transforming testosterone into estrogen, so quite obviously men have significantly more testosterone than estrogen. All according to Nature’s plan.
Nature didn’t plan the “modern” diets still followed by many. Most modern diets stimulate much more insulin secretion than hunter-gatherer diets. As you read above, “modern” diets stimulate very much more insulin in “triple-fat-gainers,” and ever more than that as the years go by.
More insulin makes the aromatase enzyme go faster and faster, turning more and more testosterone into estrogen. This impacts men more noticeably than women; as more estrogen is made, things don’t work as well for men in the sexual function department. Higher than usual estrogens aren’t good for prostate glands, either. In severe cases, men develop “man boobs”!
More insulin makes a woman’s aromatase enzyme go faster too, with the same result. More estrogen is made, less testosterone left behind. To quote a well-known politician, “What difference does that make”? As in that politician’s case, it makes quite a difference.
For some (but certainly not all) women, testosterone is important for libido. As muscle is just as testosterone-dependent in women as in men, less testosterone means less muscle mass, significantly raising risk of becoming a “little old lady.”
It’s not as well known that women’s moods are not just affected by estrogen and progesterone, but also by testosterone and DHEA, the “adrenal androgen.” One of Tahoma Clinic’s medical assistants told me she could tell when women using bio-identical hormone replacement were using adequate androgens “because they quit calling me on the ‘phone all the time!”


Remember, the unique metabolic difference between “triple-fat- gainers” and others is a significantly higher-than-usual insulin response to even one day’s worth of carbohydrate intake. Sooner or later, that unusually high (and now every day high) insulin response causes “metabolic syndrome”, sometimes starting as early as childhood. (Quick review: “metabolic syndrome” is defined as a combination of two or three or all four of the following: high blood pressure, high cholesterol, abdominal obesity, and the recent (research-proven[viii],[ix],[x],[xi]) addition of osteoarthritis, which is also called degenerative joint disease). “Triple-fat-gainers”—almost always children and younger adults—who don’t already have “metabolic syndrome” will almost certainly develop it if they (or their parents) don’t recognize what’s happening and take steps to prevent it.


So what to do? Treat the cause, not the symptoms! Patent medications to lower cholesterol and blood pressure do nothing at all to get at the cause of metabolic syndrome, that persistently high insulin signal. To reduce that now-persistently-high insulin signal (worst in “triple-fat-gainers”) stimulated by eating way more carbohydrates (starches and sugars) than were ever available in “hunter-gatherer” times, the only program that can possibly (and safely) treat the cause is a return to a low-carbohydrate, “hunter-gatherer” type diet (Paleo Diet) along with “hunter-gatherer” type exercise (termed “interval training” in modern times).
If done strictly, this will actually eliminate the cause of the “metabolic syndrome” and simultaneously prevent type 2 diabetes. Yes, there are supplements that will help the process (more about those in another issue), but without strict adherence to the very specific “caveman” (and of course “cavewoman”) diet and exercise programs, these supplements can’t do the job.
For many, it’s not easy to make these changes, but when they’re adopted, they work. Metabolic syndrome slowly disappears. Type 2 diabetes is prevented! No patent medicines required! And as a bonus for “triple-fat-gainers”, they lose all that excess fat! A small bonus point: Almost all “triple-fat-gainers” who’ve followed the Paleo Diet and exercise program have told me they’ve been able to eat as much as they want and continue to lose weight if everything they ate was “in the Paleo book”.
Other Articles In This Edition of Green Medicine

[iii] Cholerton B et al. Insulin Resistance and pathological brain aging. Diabet Med 2011
[iv] Fried SK et al. Regulation of leptin production in humans. J Nutr 2000
[v] Habib CN et al. Leptin influences estrogen metabolism and accelerates prostate cell proliferation Life Sci 2015
[vi] Dondi D et al. Estrogen receptor β and the progression of prostate cancer: role of 5α-androstane-3β, 17β-diol. Endocrine-Related Cancer 2010
[vii] Healy LH et al. Metabolic Syndrome, Central Obesity and Insulin Resistance are Associated with Adverse Pathological Features in Postmenopausal Breast Cancer Clin Oncol 2012
[viii] Korochina IE, Bagirova GG. [Metabolic syndrome and a course of osteoarthrosis]. Ter Arkh. 2007;79(10):13-20. [Article in Russian]
[ix] Korochina IE. [Determination of C-peptide, serum insulin, and characteristics of tissue insulin resistance in patients with osteoarthrosis]. Klin Lab Diagn. 2008 Jul;(7):18-22. [Article in Russian]
[x] Puenpatom RA, Victor TW. Increased prevalence of metabolic syndrome in individuals with osteoarthritis: an analysis of NHANES III data. Postgrad Med. 2009 Nov;121(6):9-20.
[xi]Velasquez MT, Katz JD. Osteoarthritis: another component of metabolic syndrome? Metab Syndr Relat Disord. 2010 Aug;8(4):295-305.

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