Use Caution when Prescribing Entyce (capromorelin oral solution) for Feline Use

Our cat, Tabatha, should be quite familiar to those reading this blog. Tabatha has been part of our family for nearly 16 years and, as such, she has grown quite attached to us. Because she’s elderly and seems more comfortable with us than with a pet sitter, we decided to take her with us on a lengthy car trip over spring break this past March. This was a bit of an experiment because, prior to this, Tabatha had typically been in the car only to and from the vet. This would be, by far, the longest car trip she had ever taken.

Tabatha seemed to be doing well on the trip and seemed to be relaxed and happy. However, much to our alarm, halfway through our road trip Tabatha suddenly stopped eating. All attempts to bribe her with various foods failed. After she had fasted for 36 hours we became quite concerned. (Cats do not tolerate periods of fasting very well. It’s very easy for cats who have not eaten to suffer from a potentially fatal condition known as feline hepatic lipdosis, which is caused when the liver’s function is compromised by a buildup of fat cells.)

Alarmed by her continued fasting, we sought help from an emergency vet clinic that we found on our route. The wonderful folks at the clinic ran a bunch of tests and decided that Tabatha had stopped eating due to stress from the road trip. Because we had another day’s travel, we had to do something to compel Tabatha to eat. The veterinarian suggested that we try treating Tabatha with a relatively new medication, Entyce (capromorelin oral solution). Entyce is a medication that has been FDA approved only for use in stimulating appetite in dogs, typically for dogs whose appetite has been suppressed by other therapies, such as chemotherapy. Entyce stimulates appetite by binding to certain receptors in the brain. The veterinarian’s thinking was that prescribing Entyce for Tabatha might effectively stimulate her appetite as it does in dogs. (While Entyce has been approved only for use in dogs, it’s not uncommon for medications to be prescribed “off label,” for various other uses. This is true for human medications, as well.)

The Entyce worked like a charm. Within hours Tabatha was eating like a lumberjack. We gave her one dose a day for three days, just as prescribed. The rest of the vacation was uneventful, even the long drive home. We were very relieved that Tabatha tolerated the trip home and we figured that her stress on the outbound trip was solely because she hadn’t traveled that far before.

Fast forward five months and it was time for another road trip. This time just as long, but in an entirely different direction. Because Tabatha had done so well on the return trip during spring break, we decided to take her with us again. We explained her history to our local vet and obtained another prescription for Entyce to take with us, just in case she stopped eating again.

As it turns out, Tabatha did stop eating again, just as we reached our destination. Fortunately, we had the Entyce with us and we gave her the first daily dose, shortly after dinnertime. We were relieved to see her eat some dinner a few hours later.

The following morning we didn’t see Tabatha up and around so we went searching for her to offer her breakfast. To our horror, we found her on her side, under a bed, staring unblinkingly as she lay motionless. We picked her up and examined her and she was completely limp. She was alive but it appeared that she had suffered a massive stroke and was completely unaware of her surroundings. We quickly got online, found the nearest emergency vet, and whisked her there. Their initial diagnosis was that she had suffered a massive stroke. The only way to be sure, they said, was to perform an MRI. The challenge, however, was that a cat of Tabatha’s age (especially one with a heart murmur, which Tabatha had developed in recent years) needed full cardiac workup before they would feel comfortable administering the general anesthesia necessary to perform an MRI on a cat. The cardiac workup, including an EKG and consult from the cardiologist, took a few hours, with us agonizing all the while over Tabatha’s unresponsive form.

By late morning, it appeared that Tabatha was a little more responsive. She was raising her head and seemed to recognize us. One possible explanation, the vet said, was that she was stabilizing a bit after her stroke. As we continued to wait or the report from the cardiologist we noticed that Tabatha continued to improve. By early afternoon she was attempting to stand.

At this point, because she was showing steady improvement, we decided to watch her overnight instead of subjecting her to the risk of the general anesthesia and the MRI. We decided to take her home to watch her so that she wasn’t in an unfamiliar place all night. We told ourselves that if she took a turn for the worse we could zoom back to the emergency vet.

To our incredible amazement, by early evening Tabatha was 90% better and the following morning she was perfectly fine.

This was no stroke. Nobody, human or animal, is perfectly fine 24 hours after a massive stroke. This had to be something else. But what?

We think it was the Entyce.

Even though Tabatha tolerated Entyce perfectly in March, we think that this time Entyce caused a reaction that mimicked a stroke.

Remember, this is a medication that was created for dogs and has been officially approved only for dogs, so there’s not much history with the off label use of Entyce with cats.

I researched the issue and only found one other person who reported this same result; however, based upon her comments, it appears that neither she nor her vet made the connection between the Entyce and the stroke-like result.

I offer this story as a caution against the off-label use of Entyce in cats. Entyce may work wonders in dogs that need their appetite stimulated, but it doesn’t appear to be suited for use in felines.

“Fat Head Kids” by Tom Naughton

I remember my elementary school teacher handing out ditto-machine[1] outline drawings of the “Four Food Groups” for us to color (within the lines, of course). By my skillful hand, dull outlines of dairy products, meats, fruits & vegetables, and grains became artwork destined for the Louvre, or at least for the front of our refrigerator. I remember, too, that my mother, wittingly or unwittingly, packed lunches that tended to include the four food groups. A sandwich on white bread, an apple, some potato chips, and maybe a Chips Ahoy cookie was the typical fare. All of it washed down with a couple of cartons of milk (typically chocolate) at the wallet-busting price of $0.06 per half-pint.

Elementary and middle school peppered us with the “Four Food Groups” messages using every medium available to 1970’s educators. By the time we entered high school, we had heard so many times that we should include foods from each food group in every meal that we were numb to the message. The bigger problem, however, was that the message was shallow and wrong. The four food groups were politically-driven—“dairy” at the behest of the dairy industry, with obvious intentions; “grains” at the insistence of the USDA, whose stated goal is to promote the sale of grains; and who knows what other puppet masters behind the scenes? For all its intense repetition, the pyramid-shaped nutritional messages beamed into our brains had very little to do with our health and far more to do with politics and special interests.

Fortunately, the days of special interests and politically-driven nutritional advice are behind us. The guidance given to our school children by educators and nutritionists today is based upon sound science and is focused solely on what is best for the children.

No, of course it isn’t.

The nutritional advice today is even more of an abysmal joke than it was in the 1970’s. The faces have changed (the four food groups have given way to “My Plate”) but politics, bad science, and special interests are even more pervasive (and insidious) than they were decades ago.[2]

Here we are, more than 40 years later, and our society still cannot manage to produce instructional material to teach our children the fundamentals of how the body responds to eating well versus eating poorly and what the principles of a healthful diet entail.

Until now, that is. And it took Tom Naughton to do it.

Entitled Fat Head Kids—Stuff About Diet and Health I Wish I Knew When I Was Your Age, Tom Naughton’s latest creation is, quite literally, the book I wish I had read when I was in middle school.[3] Moreover, it’s the book about nutrition that I wish everyone had read in middle school. If they had, we probably wouldn’t be a nation of obese, diabetic, heart patients today.

Unlike the USDA’s “My Plate” drivel that tries to appeal to youngsters but falls painfully short, Fat Head Kids is fun and engaging from the beginning. And by “beginning,” I mean the cover itself. Illustrated by Tom’s wife Chareva, Fat Head Kids‘ illustrations enhance Tom’s already excellent content.

Naughton’s book begins by attacking the “gluttony and sloth” model of obesity, wherein the overweight are shamed into believing that losing weight is a matter of will. Naughton uses this initial chapter to introduce, and dispel, the simplistic calories-in/calories-out model that has caused so much frustration to so many. Assuaging the reader’s “guttony and sloth” guilt at the beginning of the book is a wise and considerate move.

Utilizing a lighthearted, space-themed approach, Fat Head Kids then introduces the reader to the spaceship Nautilus, a mechanical analogue to the human body. The Nautilus, along with entertaining characters that include a pointy eared canine science officer named Mr. Spot and the ship’s doctor, Dr. Fishbones, teaches the science behind healthy and unhealthy eating. The science is approachable and does a wonderful, and all too rare, service to the book’s adolescent audience: It treats kids like they have a brain. Instead of simply hammering an unsubstantiated “eat this, not that” message, Fat Head Kids makes a scientific case for eating well and an equally compelling case against eating the way today’s “experts” endorse.

Journeying through space on the Nautilus, we not only learn about the science of healthy and unhealthy eating, we learn about the politics of nutritional advice and about the social and political forces that drove scientists away from the scientific method and into the arms of special interests and misguided love for failed theories. Once again, Naughton strives to inform his reader, rather than offer unsubstantiated dogma like the kind that has, for too long, passed for science.

Wisely, Naughton concludes Fat Head Kids with a chapter entitled It’s Perfectly Good to be Good Instead of Perfect. Espousing a “perfect is the enemy of good” philosophy, the last chapter reminds the reader that simple changes, like avoiding refined sugars, vegetable oils, and grains, will have a profound impact on one’s life. Naugton reminds his young readers that life is a journey to be savored and cherished and worrying about having a perfect body or looking like a supermodel isn’t what’s important about life. Having a body healthy enough to enjoy life is what’s important.

I’m thrilled that Tom Naughton has written Fat Head Kids. Nature, they say, abhors a vacuum and there is indeed a vacuum in the world of sage nutritional advice for adolescents. Kids today are too sophisticated for superficial advice without merit or substantiation. Fat Head Kids teaches, not preaches.

I hope this book becomes part of every middle school curriculum. At the very least, I hope it flies off the shelves and finds its way into households all over the modern world.

And in a final note: During the recent Low Carb Cruise lecture series, Tom previewed an animated version of Fat Head Kids that is planned for release this fall. If you liked the style of the movie Fat Head and you love the content of Fat Head Kids, you’re going to love the movie Fat Head Kids. (And the highest praise I can offer is that Fat Head Kids, the movie, scored very favorably among the middle school-aged movie reviewers that I spoke to on the cruise.)

Fat Head Kids cover

Fat Head Kids is the book I wish I had read as a kid.




[1] Those of you who remember a ditto machine probably remember staying within the purple lines while coloring various drawing sheets that the teachers handed out. Learning about money? Color a ditto machine page featuring outlines of money. Learning about mammals? Color a ditto machine page of lions and tigers. You get the idea. And, of course, the favorite part of the day was the mildly hallucinogenic odor of the freshly printed ditto machine pages.

[2] I say more insidious becuse I don’t recall experts in the 1970s recommending statins for school children.

[3] Those of you familiar with my work know I’m a fan of Tom Naughton. I became a fan of his after seeing his wonderful documentary “Fat Head” and even more of a fan after getting to know him and learning what a great guy he is. When I wrote my book, “Don’t Die Early,” Tom reviewed it very favorably and he’s blogged for years, serving a wealth of information to his followers on diet, nutrition, and the politics of food. This is all to say that I’m certainly biased in favor of Tom and his work. That said, if I didn’t like “Fat Head Kids” I’m certainly not going to say otherwise.

FDA Approves Enrichment of Corn Masa Flour with Folic Acid

At the urging of groups like the March of Dimes, who seek to reduce the incidence of birth defects in the United States, the FDA last month issued approval for manufacturers to enrich corn masa flour with folic acid. (After much discussion and contention, the FDA mandated in the 1990’s that wheat flour be enriched with folic acid.[i])

The specific goal of those advocating folic acid enrichment is to reduce a specific class of birth defects known as “neural tube birth defects,” those defects arising from malformation of the brain, spine, or spinal cord. Neural tube birth defects include spina bifida, anencephaly, and cleft palates, and are a class of birth defects that are most strongly linked to a deficiency in dietary folate (not folic acid; I’ll explain that in a moment).

The logic here is that corn mesa flour is an increasingly prevalent staple of the American diet and enriching it will further reduce birth defects, especially among the Hispanic population.

There are times when public medical policy is based upon what is expedient, not what is ideal. I think this is one such example and I’m troubled and conflicted by it.

On one hand, who doesn’t want to reduce birth defects? Birth defects, especially neural tube defects are heartbreaking, crippling, and even fatal. Only a heartless ogre would say, “Nah, I’m not interested in reducing birth defects!”

What troubles me is not the goal, it’s the use of folic acid to get there. Folic acid, you see, is a synthetic folate that is unusable by the human body. Folic acid must be converted by the body into folate before it is biologically useable.

Folic acid that is not converted is unusable and, research is showing, is harmful:

One animal study showed that rats given excess folic acid during pregnancy gave birth to offspring that exhibited metabolic dysfunctions, including insulin resistance and obesity.[ii] Additionally, human studies show that excess folic acid increases the incidence of asthma in offspring.[iii] Other studies show that folic acid taken at just two times the recommended amount during pregnancy promotes the growth of existing pre-cancerous or cancerous cells in the mammary glands of rats. Clearly, animal and human studies are giving reason to believe that synthetic folic acid can be harmful if taken even to slight excess during pregnancy.

In the words of one of the folic acid researchers, Professor Elisa Keating, “our study shows that it is possible to have too much of a good thing…the search for a safe upper dose of folic acid is urgently needed.”

Note that the researchers are talking about folic acid, not about folates. It’s impossible to “overdose” on green vegetables and ingest too much folate. Folates are naturally occurring, easily metabolized, and safe at any realistically possible intake. Folic acid, on the other hand, is artificial, must be converted in the body, and is not safe when taken to excess.

Complicating the discussion of safe folic acid intake is the genetic variability between individuals when metabolizing folic acid into folate. This conversion is dependent upon an enzyme that our body produces and, depending upon one’s genetic variability, one can convert folic acid to folates rather easily or rather poorly.[iv] As many as 50% of people in the world today have a variation that makes folic acid conversion less efficient, making harmful buildup of folic acid more likely. Those most likely to have the variation that most impedes folic acid conversion are those of Italian and of Hispanic descent.

As I’ve advocated many times before, from inflammatory response to blood glucose elevation to the presence of agents like glyphosate, there are plenty of reasons to avoid grains altogether, especially wheat and corn. With the enrichment of corn masa flour with folic acid, however, there’s now one more reason to avoid corn. The better way to get one’s folates is to avoid folic acid altogether and eat naturally occurring, green leafy vegetables that contain natural folates.

Therein lies the expediency of the folic acid enrichment policy. Is it reasonable to say to the public, “Just get all your folates from green vegetables? Don’t eat corn or wheat at all.” How many will follow such advice? I can promise you that very few will. Our nation’s rates of obesity, inflammatory disease, heart disease, and diabetes are a testament to that. And without the dietary enrichment of folic acid, the birth defect penalty will be exacted upon those without a voice in the matter: the child in the womb.

So, I guess my opinion boils down to this: if you’re pregnant and insist upon eating grains, it’s probably better that your grains have some folic acid in them than not. Do not, however, tell yourself that you’re doing anything optimal. You’re just doing something marginally less harmful. Much the same as if you tried to convince yourself that smoking filtered cigarettes is good for your baby because it’s much better than smoking unfiltered ones.





[iv] The variability in folic acid metabolism is centered on the MTHFR gene. Those with the most serious conversion impairment are advised to avoid folic acid altogether. The MTHFR variability, or mutation as some call it, is a topic worthy of a much larger discussion. If you’re interested in learning more, I suggest you start at

Make Time for Sunshine

If you read Don’t Die Early, you know I’m a firm believer on the benefits of adequate levels of vitamin D. I learned a great deal about vitamin D by reading the writings of Dr. John Cannell, who founded the Vitamin D Council as a non-profit organization dedicated to teaching the world about the importance of adequate vitamin D levels. As Dr. Cannell attests, and many researchers and practitioners are learning, vitamin D has far-reaching implications for an amazing array of conditions affecting us today, including heart disease, MS, and Alzheimers.

I’m very pleased to see more and more studies showing the benefits of maintaining vitamin D levels, even if it means (gasp!) spending time in the sun on a regular basis.

The first study that caught my eye was published last month in the Journal of Internal Medicine. In this study, researchers studied 30,000 Swedish women for 20 years, correlating sunlight exposure to overall mortality. In the words of the researchers, avoiding the sun “is a risk factor for death of a similar magnitude as smoking.” Read that again: avoiding the sun causes as much harm as smoking. Specifically, the researchers showed the women who avoided the sun not only died earlier, but they also had a higher incidence of a number of diseases, including cardiovascular disease, diabetes, and multiple sclerosis. The study was also able to show that the benefits of sunlight exposure increased in proportion to the amount of exposure—the more time in the sun, the less likely the participants were to suffer the diseases cited.

The next three studies all discuss vitamin D in the context of multiple sclerosis, both in treating and in preventing.

In the study Vitamin D Status During Pregnancy and Risk of Multiple Sclerosis in Offspring of Women in the Finnish Maternity Cohort, Finnish researchers identified individuals with MS and examined blood samples that had been taken from their mothers during the pregnancy and stored. The researchers found that, as compared to non-MS control group, mothers with those who developed MS were twice as likely to be vitamin D deficient. Past studies have shown little or no correlation between vitamin D levels during pregnancy and the risk of MS, but researchers observed that previous studies suffered from limitations of poor controls and small sample size.

Researchers have a number of theories to explain why low vitamin D levels increase the risk of developing MS, including vitamin D’s suppression of pro-inflammatory T-cell populations and the critical role that vitamin D plays in the formation of myelin.

As many will point out, however, correlation is not causation and to fully understand the role that vitamin D plays in prevent MS, it’s important to try and identify whether vitamin D deficiency is simply correlated with increased risk of MS or if it’s truly part of the cause.

To help show that the vitamin D connection with MS is causal (that is, actually is a cause and not just an unrelated correlation), another study examined those with genetic anomalies that produce low vitamin D levels to see how their low D levels correlate with increased risk of MS. The thinking here is: because the low vitamin D levels in these individuals are genetic, there are no lifestyle factors that might complicate the picture. In other words, if there’s an increased risk of MS among everyone with genetically low vitamin D, it gives strength to the argument that the vitamin D levels are playing a role because the various lifestyle factors among those studied will be randomized and will cancel out.

What did these researchers find? Much the same as other research: Those with genetically low vitamin D levels had twice the risk of developing MS.

And what about those with MS? Can vitamin D possibly bring some benefit? Researchers at Johns Hopkins say “yes,” it can. By supplementing MS sufferers who have low vitamin D levels for a period of six months researchers checked the patients’ blood and found “pleiotropic immunomodulatory effects” in the blood of those receiving therapeutic vitamin D dosages. (“Pleiotropic immunomodulatory effects” is a mouthful, but in this usage it means that the vitamin D supplementation brought multiple beneficial changes to the immune system that reduce the attacks on the MS patients’ nervous system.)


This is just a few articles released quite recently but there’s no shortage of research showing the benefits of vitamin D, best obtained by responsible sunlight exposure (“responsible” means don’t let your skin burn) and absent sunlight exposure, via vitamin D supplementation.

When I think of Dr. Terry Wahl’s completely reversing her MS with dietary changes and all of the research showing the benefits of sun exposure and vitamin D, it only reinforces what I already believe: good food that is devoid of grains, sugars, vegetable oils, and other toxins, coupled with time in the sun and fresh air, are some of our best preventive medicine tools.

Ok. I’ve spent enough time in front of my computer. It’s time for a walk in the sunshine.


Step Right Up and Play the Statin Lottery

An article published on Medscape yesterday caught my eye. The article, Should Clinicians Change How They Talk Statins with Patients? New Study Says Yes, reports on a new statin study and in doing so, echoes the argument put forth in the study that patients would be more responsive to statin usage if the gains were presented “in the language of lotteries,” and patients were enticed by “the possibility of a bigger payoff.”

The Medscape article discusses a study in the medical journal Open Heart, which argues that even though research show a trivial “mean lifespan gain,” on average, among groups of people taking statins, there are some patients who benefit greatly from statin usage. To reach this conclusion, the researchers looked at a large population of statin users and divided the participants into two groups:

  • Group 1: the 93% of statin users who have the worst gain in lifespan (7.4 months on average)
  • Group 2: the remaining 7%, who show an average of 99 months extended lifespan.

By dividing the group of statin users in this way, researchers argue that practitioners can present statins in a more exciting and appealing way.

Quoting the lead researcher of the study, Dr. Darrell Francis of the National Heart and Lung Institute in London,

“Many patients want to know ‘What’s the size of the jackpot?’ So when talking to patients, maybe we really should use the language of lotteries.”

Yes, lotteries! You know, that game where most everyone spends their money and gains nothing and some statistically insignificant few win big? Yeah, that’s what medicine is becoming, all in the name of selling statins. Only in this “lottery,” the losers suffer more than the loss of a few dollars: statin users lose their memory funding a multi-billion dollar industry, increase their risk of cancer and diabetes, and suffer a host of other complications that are readily downplayed by the statin-fueled medical establishment that’s hell bent on selling more statins.

And, of course, as is common when the medical establishment discusses statins, this “lottery” approach comes complete with a way to obfuscate reality. According to the researchers, practitioners should consider saying only that there is a “chance of a 10-year* life-expectancy extension” from taking a statin but physicians should not reveal the actual chance of seeing any benefit unless the patient asks, because “…most people are very interested in the size of the payoff and not the probabilities,” Dr. Francis observes.

Psychology researchers describe lottery gambling as “paradoxical behavior” because those who buy lottery tickets are compelled to “go for the win” even though it’s obvious that the odds overwhelmingly favor the house. Many others aren’t so kind when describing the growing practice of state sponsored gambling, calling it “predatory” because it plays upon the public’s desire to win big, no matter the odds. Psychologists have coined the term “lottery mindset,” to describe the average person’s common propensity for ignoring the odds while focusing only on the payoff.

I find it deplorable that these predatory tactics are now being advocated to sell more statins. It appears that this is the new practice of medicine: If the science doesn’t hold water, resort to deplorable, predatory psychological manipulation.

When I weigh the statin risks and side effects against the statistically insignificant benefits that statins offer (benefits that are easily duplicated by lifestyle changes to control inflammation, glycation, and oxidation), I think equating taking statins to playing the lottery is not the ideal analogy. Russian Roulette seems more accurate to me.





* The study cited a 99 month average life extension for those select few who were “winners,” not 10 years. In typical statin numerical manipulation, the pro-statin crowd immediately rounded 99 months (8.25 years) to 10 years, giving themselves an instant 21% false gain.

Interviewed on Wendy Myers’

I had the great pleasure of meeting Wendy Myers on the recent Low-Carb Cruise. Her presentation on Obesegens: Chemicals That Make You Fat was an eye-opening overview of the many disruptive chemicals in our environments and in our foods.

My subject of my talk on the Low-Carb Cruise was the legislative, economic, and sometimes violent attacks against America’s independent farmers. After the cruise, Wendy asked if she could interview me for a video podcast on her web site and the podcast has been posted, video and text. (You won’t hurt my feelings if you read the transcript instead of suffering through my first video podcast.)

Thanks again to Wendy Myers for the interview! While you’re there, check out the great information throughout

Another Strike Against Monsanto’s Roundup

Unless you’ve been living under a rock for the past few years, you’re undoubtedly aware of the controversy surrounding Monsanto’s Roundup (glyphosate) weed killer. Roundup is a principal component of Monsanto’s GMO (genetically modified organisms) policy in which crops (primarily corn and soy) are genetically engineered to be resistant to glyphosate toxicity, which is lethal to virtually every weed known. By planting glyphosate-resistant crops and then spraying liberal amounts of glyphosate, growers can (allegedly) grow crops more economically, burdened far less by weed growth. In addition to using glyphosate on GMO crops, some of these farmers are also using it as a “burndown” herbicide to eliminate weeds prior to planting. The use of glyphosate as a burndown agent is apparently quite prevalent when growing wheat.

Setting aside the emerging issues of glyphosate-resistant super weeds that are now appearing and doubling every two years, there has been much controversy in recent years over the toxicity of glyphosate in humans.

One glyphosate study, performed by Dr. Andreas Carrasco and a team of researchers in Argentina, analyzed birth defects in frogs and chickens exposed to glyphosate. His study revealed the same skeletal deformities in these animals as was witnessed in the children that were born to the mothers who lived in agricultural communities where large amounts of glyphosate were being aerially applied to glyphosate-resistant GMO soybeans.[1]

A team led by Dr. Gilles Eric Seralini documented severe damage from glyphosate to umbilical cord cells from human infants. Glyphosate residue kills both the sperm and the egg at a half part per million and causes endocrine disruption to the cells at 0.2 of a part per million.[2]

Monsanto has steadfastly held that glyphosate is harmless, even falsely claiming that glyphosate doesn’t cross the placental barrier to reach the fetus, a claim readily disproved by the journal Clinical Research in Toxicology.

Adding to the mounting pile of evidence that Monsanto’s glyphosate is harmful is MIT researcher Stephanie Seneff, who focuses primarily on the relation between nutrition and health.

In a June, 2014 slide show that is quickly becoming famous, Dr. Seneff shows disturbing correlations between the increasing use of glyphosate and a number of maladies, including autism, dementia, celiac disease, non-Hodgkin’s Lymphoma, and intestinal infection. More than just showing correlation, Dr. Seneff offers some possible mechanisms of action that explain glyphosate’s role in promoting these increasingly common diseases. For example, Monsanto argues that a principal mechanism of glyphosate’s action, the disruption of the Shikimate pathway (a biochemical process used by plants and bacteria to generate the amino acids: phenylalanine, tyrosine, and tryptophan), is harmless to humans because humans do not utilize the Shikimate pathway. What Monsanto is conveniently overlooking, however, is that human gut bacteria does use this biochemical process to produce amino acids, and other biochemical goodies, that are vital to human health, which produces a shortage of neurotransmitters and folate.

Dr. Seneff’s also points out that because glyphosate’s damaging effects increase over time, most studies are too short to show damage. (If you’ve read “The Truth About Drug Companies” by former New England Journal of Medicine editor-in-chief Dr. Marcia Angel, you’re quite familiar with the ways that drug safety trials are often carefully trimmed to avoid showing harm. If, for example, a medication being studied begins to show harm after 24 weeks of use, the drug company can publish the results of the trial, shortened to 22 weeks long, showing that the medication produced no ill effects. It’s not hard to imagine a pesticide or herbicide safety studies being manipulated in the same way.)

Perhaps most alarming is that glyphosate long-term safety studies do not include the additives (also known as adjuvants) that are mixed with commercially applied glyphosate. Why is this alarming? Because according to the journal BioMed Research International, in 100% of the cases where adjuvants are used in pesticides, they increase the toxicity of the principal ingredient, making the principal ingredient as much as 1,000 times more toxic.

To drive the point that there’s a correlation between glyphosate use and autism, Dr. Seneff shows this rather alarming graph:

Glyphsate and Autism

While any reputable researcher will tell you that correlation is not causation (a chant that’s becoming all to familiar in the blogosphere), correlation does accomplish one thing: it points to investigative avenues that are potentially worth exploring. Dr. Seneff points out that even a casual exploration reveals that the following biomarkers for autism can all be explained as proven effects of glyphosate on biological systems:

  • Disrupted gut bacteria; inflammatory bowel
  • Low serum sulfate
  • Methionine deficiency
  • Serotonin and melatonin deficiency
  • Defective aromatase
  • Zinc and iron deficiency
  • Urinary p-cresol
  • Mitochondrial disorder
  • Seizures; glutamate toxicity in the brain

Take a look at Dr. Seneff’s slide show and see if you agree that it’s time we spend some real, unbiased time looking at the effects of glyphsate on all of us and stop believing Monsanto’s propaganda.

And while you’re at it, consider making a donation to Food Democracy Now to aid in their fight for GMO labeling so that no matter your position on GMOs and glyphosate safety, you can make an informed purchasing decision when deciding what to feed yourself and your family.



[1] Paganeli, A, et al., Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chemical Research in Toxicology 2010;23:1586–1595.

[2] Benachour, N, et al., Time- and dose-dependent effects of Roundup on human embryonic and placental cells. Archives of Environmental Contamination and Toxicology Journal. 2007;53:126–133.

Medical Experts Once Again Helping People Become Diabetic


Yet another absurdity in diabetes advice comes from the staff at Harvard Medical School and it illustrates quite nicely why we have become a nation of diabetics.

In an article entitled Sugar’s Role in Diabetes (on a web site with the laughable title Better Medicine), physician author Robert Shmerling argues that elevated blood sugar levels are the result of having diabetes, not the cause.

Improved blood sugar control may reduce the chances that certain complications of the disease will develop. But just because the disease is characterized by an elevated blood sugar level and because lowering the blood sugar level is an important goal of therapy, a high-sugar diet does not cause the illness. An elevated blood sugar level is a result of having diabetes, not the cause.

Dear Dr. Shmerling: I’ve got news for you: Elevated blood sugars are both. They are the result of diabetes and a significant cause.

In his own definition of Type 2 diabetes, Shmerling states:

…the body’s tissues become resistant to insulin, requiring more insulin than the pancreas can produce to keep the blood sugar normal (type 2 diabetes).

What does he claim causes a person’s tissues to become resistant to insulin?

He says that heredity, obesity, and medications are the culprits.

Here’s a CDC graph showing the growth of diabetes in America:


While I’m sure genetic factors play a role in determining the likelihood and the rate at which one develops Type 2 diabetes, is he really arguing that our population’s genetics have changed so dramatically during this time as to explain this rise in diabetes?

In other words, a rapid and unexplained genetic shift in the modern world’s population, not diet, is causing the incidence of diabetes to skyrocket?

Uh, ok. Sure, doc.

I would have to practice in front of a mirror so that I could say that without bursting into laughter.

And, medications? Please tell me what medications have caused such an alarming increase in diabetes over the past 50 years. The attorney general in every state in America would like the answer to that question, too.

And finally, Shmerling states that obesity causes diabetes. I knew that one would rear its head soon enough. That’s laughable from a man that states:

Assuming an elevated blood sugar level is the cause of diabetes is like assuming that coughing is the cause of pneumonia.

Let me channel Dr. Shmerling:

Assuming that obesity is the cause of diabetes is like assuming that coughing is the cause of pneumonia.

Obesity isn’t the cause of diabetes, it’s simply another result of insulin resistance and elevated glucose levels.

Shmerling seems to have forgotten that elevated insulin levels trap fat in fat cells, preventing weight loss.

In my book, Don’t Die Early, I talk about the effects of insulin on weight retention:

“It may seem unbelievable that having an elevated insulin level could prevent the body from burning fat when we’re hungry, but it’s true. Insulin is amazingly powerful at keeping fat locked into fat cells where it remains inaccessible and cannot be metabolized for energy. How powerful? Obese rats that are given insulin injections to maintain high insulin levels and then put on a starvation diet remained obese while dying of starvation. These starving, yet obese rats digested their own muscles and organs for food until they died from starvation, without losing any of their body fat.

“Yes, even though they were starving, the elevated insulin levels prevented their body from metabolizing fat from their fat cells for energy, forcing their bodies to digest their own organs and muscles for nourishment. Think about this the next time you wonder why people can’t lose their unwanted body fat even though they are not eating much. It’s very likely that the foods that they are eating are causing a large insulin response, which is keeping the fat locked into their fat cells.”

And while we’re on the subject of weight, Shmerling states:

And not all persons with diabetes are overweight — that’s another myth. For these patients, heredity and perhaps other undiscovered factors are more important.

Dr. Shmerling, let me explain the “mystery” of why some diabetics are thin and some are not. (Again, I’m quoting my own book. Sorry to be so self-serving here, but I wrote this book to help enlighten people about the causes of diabetes and other maladies affecting us today. I didn’t think Harvard Medical School staff members were part of my target audience.)

“The most surprising thing about the effect of insulin resistance and trapping fat in fat cells is that despite what I’ve just said about this effect, we cannot determine how insulin-resistant we are by how much extra fat we are carrying.

“While it’s true that an overweight person is almost certainly insulin-resistant, a thin person is no less likely so. Why is this? It’s because fat cells can become insulin resistant at different times in different people. If you’re “lucky” enough to have fat cells that become insulin resistant quickly, before they expand considerably, then you’re a thin, insulin-resistant person, subject to the same damage from elevated glucose and insulin levels as an obese insulin-resistant person.

“Everything I’ve said in this section about fat being trapped in fat cells and about a person becoming hungry every couple of hours and spending the majority of the time with elevated glucose and insulin levels can be just as true for a thin person as for an overweight person. In fact, it’s probably the thin person who is less fortunate when it comes to insulin resistance because the thin, insulin-resistant person’s diabetes will go undetected far longer, due to the false sense of security that being thin brings.”

So back to the original question, what does cause insulin resistance, the definition of Type 2 diabetes?

Why, it’s exposure to increased levels of glucose, of course!

I’ll once again quote from my own book:

“Let’s think about the amount of glucose in a healthy, non-diabetic person. In such a person, the total amount of glucose in the blood-stream during the fasting state is less than a teaspoon (which is less than 4 grams of glucose). An 80-pound, fasting, non-diabetic child has less than one-half teaspoon of glucose.

“What do you think happens when a person eats a meal that dumps ten or a hundred times the fasting amount of sugar into the bloodstream? The body simply cannot allow the blood glucose level to suddenly become 100 times the normal fasting amount. That much glucose in the bloodstream would be acutely harmful, perhaps even fatal, if not metabolized quickly. The body reacts to elevated glucose levels by doing whatever it must do to quickly metabolize the glucose. This means secreting insulin. Lots of insulin! Way more insulin than was ever necessary for a person before the advent of refined white flour, 64-ounce sodas, tortilla chips, and candy bars. 

“Over time and with frequent exposure to high levels of insulin, the cells in the body become increasingly resistant to insulin, requiring more and more insulin to accomplish the same glucose transport functions as before.”

In other words, repeated and significantly elevated glucose levels, the levels caused by our daily diet of grains, 64-oz sodas, chips, and other crap, cause insulin resistance.

What other problems do elevated glucose levels cause?

In a sad, cruel irony, elevated glucose levels damage the very components that are responsible for producing insulin: the beta cells of the pancreas.[1]

That is, elevating one’s glucose levels causes beta cell death, which causes glucose levels to rise, thus hastening beta cell death.

It’s what I call a “shit spiral.”

But in his thoughtful assessment of diabetes, Dr. Schmerling completely ignores the role that elevated glucose levels play in damaging the beta cells of the pancreas.

Oh, I forgot. Sugar doesn’t cause diabetes.

In conclusion, Shmerling states:

…the notion that a high-sugar diet causes diabetes is a medical myth that demonstrates how the effect of an illness may be mistaken for its cause.

And I submit to you, Dr. Shmerling, that by ignoring the role of excessive carbohydrate intake in the development of Type 2 diabetes, you are propagating a horribly damaging falsehood.

The advice from physicians of your ilk are a significant factor in the rise of diabetes and the decline of this nation’s health.

[1] Gleason, CE, et al. Determinants of glucose toxicity and its reversibility in pancreatic islet Beta-cell line, HIT-T15. American Journal of Physiology, Endocrinology, and Metabolism 2000;279: E997–E1002.

This is only one of many studies showing how elevated glucose levels kill pancreatic beta cells, thus hastening the onset of Type 2 diabetes.

Lipids: How Big Their Role?

If you’ve read Don’t Die Early, you know the book explains in great detail the failings of the Lipid Hypothesis, the dangerously inaccurate model that proclaims that having “too much cholesterol” causes heart disease. Don’t Die Early explains that the real factors that combine to form heart disease are glycation (elevated blood sugar), inflammation, oxidation, and damagingly small LDL particles. These four factors are overwhelmingly more relevant to one’s risk of heart disease than simply measuring total cholesterol, or even measuring the quantity of LDL (the wrongly labeled “bad cholesterol”).

Examining these four factors, however, begs the question do they all contribute equally to heart disease? In other words, can one or more of these factors be less of a worry if others are in check?

I’ve posed this question to a number of forward-thinking[1] cardiologists and studied the work of various researchers and the answer is a definite “maybe.” And the “maybe” points at lipids.

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Budget Today for Your Future Health

A few years ago my wife and I became frustrated by Quicken’s continued decline on the Macintosh platform and, enticed by a colleague’s endorsement, we decided to try the financial software YNAB (You Need a Budget).

Unlike most other financial software, which focuses more on past spending and pays lip service to budgeting, YNAB’s unique approach to financial freedom is to stridently emphasize budgeting above all else. YNAB’s philosophy so strongly embraces honest budgeting and accountability that the ideal implementation of a YNAB budget does not allow forecasted income at all, instead structuring one’s monthly budget to spend the previous month’s income, not the current month’s income.

This paradigm shift away from “can I make enough this month to pay my bills?” into “how shall I structure my spending this month so that I can live off of last month’s income?” may take some time and sacrifice to achieve, but doing so results in a level of financial comfort foreign to most of us. It’s truly refreshing to spend with an eye towards the future instead of spending impulsively and then running a report to see how bad the damage is.

“That’s nice,” you say, but why am I talking about budgeting on a blog devoted to preventive health?

Simple. It occurred to me this evening while working in YNAB that most of us treat our health the way we treat our budget: we eat whatever we want, typically sugar, vegetable oils, and grains, and when our health slips into the red, we then talk about making changes to improve things. In other words, we treat instead of prevent.

That’s living Quicken style when we should be living YNAB style.

Imagine living a life of minimal sacrifice today that repays significant health dividends in the future. Imagine turning off the television so you can make preventive health your new hobby. So you can give up reacting to sound bites and physical maladies and truly take control of your future health.

The analogy between acting today to achieve future financial freedom and acting today to achieve optimal health as you age is a strong one. Both require some study and some effort and both can pay handsomely.

Think about “budgeting” for a healthier future. Your future self will thank you.