After treating thousands of patients over the past few decades, it became obvious to me that poor dietary choices can adversely affect brain function, leading to a disease that I call Carbohydrate Associated Reversible Brain syndrome or CARB syndrome. When I talk to my friends in academic medicine like Dr. Richard Johnson, the well-known fructose researcher, they tell me that although they think I’m right, we need more studies to support the concept. After all, suggesting that certain dietary elements are causing reversible brain dysfunction is a rather radical concept.
As a working primary care physician, I am not in a position to do such research by myself, so I have been trying to convince people in academic medicine to do research on diet and brain function. Believe me, that’s not an easy thing to do. Because pharmaceutical companies sponsor most basic research, it’s hard to find funding for studies on diet and health. I guess we can’t really expect the food or agricultural industries to sponsor this type of research—they’re too busy making money and making us sick!
Recently my friend Dr. Robert Lustig sent me an article that strongly supports the CARB syndrome disease model. The article “Obesity and Metabolic Syndrome and Functional and Structural Brain Impairments in Adolescence” was recently published in the journal Pediatrics. This study is truly revolutionary, because for the first time it documents a clear connection between diet and poor brain function.
They looked at two groups of adolescents, one group with metabolic syndrome and one group who were metabolically healthy. The metabolic syndrome is a pre-diabetic state defined by insulin resistance, low HDL (good) cholesterol, elevated triglycerides, hypertension and abdominal obesity. Metabolic syndrome up until recently has been extremely rare in young adults, but over the past few decades it has become common in this age group.
Based on research by Dr. Johnson and others, it is now clear that metabolic syndrome is primarily driven by excessive intake of the simple sugar fructose, mainly in the form of sugar or high fructose corn syrup (HFCS). Dr. Johnson has shown when you consume more than 25 grams of fructose per day, your liver begins to fill up with fat, leading to insulin resistance. Excessive fructose also increases levels of uric acid, and high levels of uric acid plays a key role in turning on your fat storage switch. To learn more about the adverse affects of fructose, I highly recommend that you read Dr. Johnson’s “The Sugar Fix” and his recently published book “The Fat Switch” available at http://mercola.com.
This study showed that the group with metabolic syndrome had a form of brain dysfunction. They had problems concentrating and focusing and their ability to perform various mental tasks was impaired. They also documented that those with metabolic syndrome had structural changes in their brains. For years we have known that diabetics suffer from similar changes in their brains, and it is now clear that the brain takes a hit long before a person develops full-blown diabetes. Our children are losing brain function because they are eating a standard American diet? This is a story that deserves to be splashed in the headlines across the world.
Sugar and HFCS don’t appear to be the only bad actors when it comes to diet and poor brain function. High glycemic carbohydrates, especially from grains, also seem to play a role in food-induced brain dysfunction or CARB syndrome. When you have insulin resistance and eat a Twinkie or similar high glycemic carbohydrate, your brain is exposed to large glucose spikes. Although neurons rely almost exclusively on glucose for their energy needs, too much glucose can damage nerve cells. That’s because unlike other cells in your body, insulin isn’t required for glucose to enter into nerve cells. When you have a glucose spike in your blood, you also have a glucose spike inside of every neuron in your body.
In this situation the glucose must be used by the mitochondria to produce energy and too much glucose releases a massive amount of free radicals, overwhelming your inherent anti-oxidant system. This leads to a condition called mitochondrial dysfunction where your mitochondria no longer function as intended. Glucose spikes also seem to lead to neurotransmitter dumping, a condition where your neurons dump out too many key neurotransmitters like dopamine, norepinephrine and serotonin. These valuable chemical messengers are normally reabsorbed by the neuron to be reused. When too many of these neurotransmitters are released at once, the reuptake system simply can’t handle the load and most of them are taken up by your blood stream and cleared by your kidneys. In other words, when you eat that Twinkie, you end up peeing away your dopamine, norepinphrine and serotonin.
When you binge on Twinkies or similar fare, you end up with a brain that is depleted of these important chemical messengers. This results in the 22 brain dysfunction symptoms that are typical of CARB syndrome. The first symptom you develop with CARB syndrome is craving for sweet and starchy foods, pushing you to consume more of the very food that is frying your brain. Is it any wonder that many of our children seem to have problems learning and functioning in an academic environment? Hiring more teachers and throwing more money at the problem will have no impact as long as we allow are children to eat this type of toxic food.
Although you may not have much control over many things in our complex modern world, you do have control over what you put in your mouth and what you feed your children. Forget about calories, because they are not relevant to the problem at hand. Focus on food composition. Eat real food, not processed food. If it has a food label, you probably shouldn’t be eating it. Eat meat, fowl, fish, seafood, vegetables, nuts and fruit. Stay away from all processed foods, sugar and HFCS. It’s a simple, not complex approach to the problem. You just need to start doing it.
Very interesting post.
While I eat nearly zero HFCS, I used to eat grains like crazy, and I think I’m experiencing what you’re describing. My brain sxs are horrible (confusion, derealization, word retrieval problems, working, short, and long term memory impairment, diminished consciousness, etc., along with endocrine issues). It’s caused me to not be able to work currently. I look forward to more posts about mitochondrial dysfunction, and also other “downstream” effects of CARB syndrome.
Thanks much for your work.
Be sure to check your thyroid function. Even with a normal TSH some people with CARB syndrome seem to benefit by taking Amour Thyroid. With CARB syndrome the brain sometimes fails to make enough thyroid stimulating hormone (TSH) to stimulate the thyroid gland to produce thyroid hormones. This results in a form of secondary hypothyroidism that cannot be diagnosed with a TSH test, the most common test used by physicians to diagnose primary hypothyroidism.
One way to assess thyroid function is to take basal body temperatures for up to 10 days. This is a link to a discussion about how this might be helpful to assess thyroid function: http://www.thyroid-info.com/articles/shames-basaltemp.htm
One of the best supplements you can take for mitochondrial dysfunction is R-alpha lipoic acid. This can be combined with acetyl-L-carnitine.
I would also suggest that you follow the recommendations outlined in my blog post. It takes time for the brain to heal, so be patient. Good luck!
Dr. Bill Wilson
Dr Wilson, I thank you so much for this post and I wish to read more about CARB syndrome in the future.
My mind has gravitating to the idea that hyperglucosis [1] would be disruptive to hormones and other biochemical messengers, and my imagination likens this to a ‘cascade effect’ where more and more hormones or messengers are knocked further away from the kind of balance, or homeostasis, they ought to be in. The longer hyperglucosis persists then the more these things will be knocked of balance, so I imagine(d).
I recall Dr Robert C Atkins was the centre of some critical attention some 15-20 years ago when his book(s) were selling well here in the UK. The detractors said his diet would to ketoacidosis. Actually Dr Atkins fully intended followers of his plan to experience the benefits of ketosis because ketosis naturally follows the process of lipolysis, and ‘lipolysis’, is the process of burning fat, which is the process every overweight person must tap into in order to shed the lbs. Ketosis and ketoacidosis, despite being similar sounding terms, are quite different things. Ketoacidosis would never be a desirable state to be in, but ketosis is the metabolic pathway via which the overweight person can lose weight, and it is, so far as we know, natural and harmless. It makes profound good sense.
If a nature equips creatures with the ability to sequester reserves of fat, as many creatures do when food is plentiful, the reserves of fat are of no real benefit unless nature provides a way to draw down from these reserves when needed. The pathway of fat sequestration involves glucosis in extremis. All this means is that under the action of insulin glucose in the blood is converted to gylcogen for storage in the muscles and liver and when those finite glycogen reserves are full then ant further excesses of glucose are converted into fats for deposition as fat.
Natures trick, seen clearly in migratory herbivores, is to permit the reserves of fat to come into their own when the grass is no longer ‘green’, but ‘lean’. As glucosis declines in its ability to meet the complete energy needs the pathway of lipolysis/ketosis starts to kick in and the creature draws down upon reserves of fat. In the human, a dietary balance that is perpetually high in carbs ensures levels of insulin are high and keeps the gate firmly closed where the pathway of ketosis is concerned. So we never get to burn sequestered reserves of fat. The solution, elegant as it is, is completely counter-intuitive and involves eating fewer carbs but a bit more in the way of fat.
Because of the brew-ha-ha surrounding Dr Atkins he was damaged goods in my mind, and despite the level of my interest I put of reading his work. But having satisfied myself being any doubt that neither saturated fat nor cholesterol are directly involved in the cause of heart disease I thought I’d give high-fat / low-carb eating a try. I hoped, as a type-2 diabetic I would ‘feel’ better; and I did. Then I felt a whole lot better when the bathroom scales indicated a loss of about 8-9 lbs over about 3-4 weeks.
Something I noted tho’ was that on occasions I awoke after a nights sleep, not feeling at all hungry, and still sensing some slight sensation of the tum being distended. Not all the content of my tum seem to have been processed, digested, and the metabolites passed over the gastrointestinal divide. So I wondered. Might the bodys’ physiology provide the means to attenuate digestion in keeping with demand on the other side of the fence, so to speak. Then if it did how would it go about this?
So there I was placing dinner plates, cups, and wineglasses in the washbowl with hot water running when I discovered we had run plain out of pot-washing detergent, goddammit. I ran the pot-cloth over them but of course the pots all came out with a film of grease all over them. The wineglasses were muckier than when they went in. How do things work in the guts?, I wondered. Would the chyme in the guts become coated with fats?, then if so do fats have mastery over the attenuation of digestion? Since bile is acknowledged as the emulsifying factor in digestion might the supply of bile be modulated, and if so, does modulation of bile attenuate the speed of digestion of gastric emptying. Dr Atkins kinda picked up on this cos he makes mention of the lessons from the concept of GI / GL and is well aware fibre attenuates digestion. But the proponents of GI / GL also suggest the presence of fat lowers the index for a given food. So there is a clue that fat attenuates digestion too.
The proposition that fat attenuates digestion in some way, and/or makes us feel fuller for longer, is very much an untamed thought for now, but it is not out of accord with what peoples experience, and Dr Atkins clinical experience tells/told them.
I have tried to search and establish what signaling molecules might be involved in reporting, control, and modulation of supply of bile but anything in proximity to endocrinology quickly becomes a minefield for a truck driver like me, but cholecystokinin (CCK) and oleylethanolamine (OEA) seem at least to be a place for inquiries to begin. I think the role of fat in gastric modulation will not have been properly explored because anything, or any work, potentially casting a positive light on fat in the diet, or casting doubt upon the lipid hypotheses, was, and is, the equivalent of professional hare-kari.
And when I looked at OEA the papers I returned via a web-search all seemed to side with the prospect of commercial appeal, as opposed to good old-fashioned good-sense. In accord, Dr Wilson, ”I guess we can’t really expect the food or agricultural industries to sponsor this type of research—they’re too busy making money and making us sick!”
I think you are right that the exit route for CARB syndrome has to be via a reduction in consumption of carbs, but not just quantity, for the GI / GL properties matter too. But likewise the addition of more fibrous types of food, and judicious inclusion of fat, could perhaps be a first-stage protocol invoked within the gastrointestinal tract that may also begin to functionally redress imbalances that persist on the physiological side of the gastrointestinal divide.
However, to place a nice ribber-stamp on affairs there needs to be a clear indication of feedback and control leading to modulation of bile that must be identified, and then only if the conditions persisting over chyme can be equated to what happens in the wash-bowl.
Notes
1, The metabolism running too much and too long on glucose from a diet too rich in carbs
Chris:
Thank you for your insightful comments. Yes it is complicated and there is a lot we don’t understand. Most of my recommendations are based on treating patients in the real world. Theories are a dime a dozen (including mine) but results are worth their weight in gold. That’s why I continue to use the CARB syndrome model–it seems to give me the most consistent positive results.
Dr. Bill Wilson
Thank you for your reply, and thank you for gracing my untamed thoughts with ‘insightful’. I agree, an ounce of results in clinical practice are worth a pound of unverified theory. And if results are seen in practice they oughtn’t be rubbished without clear reason. A lot is good sense. Diets of the past provide uncorrupted models, and it is highly likely innovations and trends in modernity are the entry point of corrupting influences that we have not evolved to be suited to. I hope my comment sounded supporting of CARB theory, for that was my intention, and I want to learn more about the disruption to the brain that CARB theory directs.
The books of Barry Sears interest me as does his discussion of the insulin – glucagon axis (I-G) and how a disrupted (I-G) balance may interfere with the balance of eicosanoids. To be fair to Barry his theory has no doubt developed over several decades but I’m currently reading a work from 1995, ‘Enter The Zone’. Barry directs that once people enter his Zone there is great reduction in the compulsion to eat, and so people don’t always feel inclined to eat their full quotient of calories. I am absolutely in accord that macronutrient balance is the key to restoring natural regulation of appetite where macronutient imbalance invokes dysregulation. Any discussion about the failure of (or inappropriate) signalling involving hormones, eicosanoids, or peptides etc., fascinates me for backing up what the evolutionary and ‘paleo’ angle may suggest.
Rather than distract from CARB theory I simply wished to offer a thought that might attach to CARB theory, that perhaps fats have been undervalued as a means, in addition to fibre, of attenuating digestion. I wonder too if satiety signals, ones that may trace back to the guts, stem mainly from fats, and if so which ones.