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APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer's by Stephanie Seneff is licensed under a Creative Commons Attribution 3.0 United States License.

Is ADHD Caused by Insufficient Dietary Fat?

Over the last few decades, there has been an alarming increase in the incidence of several syndromes that affect both the physical and mental health of children and adults, especially in the United States. These include the obesity epidemic and metabolic syndrome, the alarming rise in the incidence of autism, the steady increase in food allergies among children, and the rise in the new brain disease termed "attention deficit hyperactivity disorder." To understand what might be causing these conditions, we need to look for substantial changes in lifestyle that have occurred between the last forty years and the previous forty years.

Two lifestyle changes that occurred almost simultaneously in the late 1970's are the practices of avoiding dietary fat and avoiding sun exposure. These practices have since gained a persistent strong endorsement by our government and medical experts, which has led to the almost unshakable belief across our population that avoiding dietary fat and sun exposure are healthy choices. I believe that these practices are in fact unhealthy, and are the underlying causes of the above mentioned diseases.

While people mistakenly believe that eating fat will lead to obesity, I have come to believe the exact opposite: that not eating enough fat can lead to obesity. I have elaborated on my arguments in a recent blog post on the obesity epidemic, and associated metabolic syndrome in America, where I claim that nutritional deficiencies in vitamin D, calcium, and dietary fats can account for most of the symptoms associated with metabolic syndrome. Previously, I developed an argument that the alarming rise in the incidence of autism in America may also be attributable to maternal deficiencies in these key nutrients, especially when the pregnant mother is sufficiently disciplined to remain thin despite strong temptations to eat. In this essay, I will develop a theory that Attention Deficit Hyperactivity Disorder (ADHD), a disease that barely existed before the 1970's, but is now steadily increasing in incidence rates in the United States, is also likely caused by inadequate dietary fats, with a possible contributory role played by vitamin D deficiency.

The American medical establishment continues to aggressively promote low fat diet, while Americans continue to grow in size and the autism epidemic keeps getting worse. By avoiding fats, Americans instead tend to eat an excessive amount of high-glycemic index carbs -- highly processed foods that digest very quickly and cause the blood sugar level to spike. This eventually leads to insulin resistance and type-II diabetes. Meanwhile, insufficient fat in the diet results in an unstable supply of fuel to the heart and fat resources to the brain. The brain utilizes only glucose for fuel, but fatty acids are essential to construct its neural connections.

In this essay, I am going to develop a theory that the rise of ADHD in America is a direct consequence of fat avoidance and sun avoidance. My theory explains many observations that have been made about ADHD, including:

-- Why ADHD is much more prevalent in boys than in girls,
-- Why ADHD children tend to have stunted growth,
-- Why ADHD children suffer from sleep disorders,
-- Why ADHD children are hyperactive,
-- Why Ritalin alleviates the symptoms.

I will also explain why I think that the widespread practice of drugging children with Ritalin, while clearly effective in promoting learning in the short term, is leading to a number of looming crises down the road, including drug abuse among non-ADHD children, and serious health issues later in life, such as heart disease and Parkinson's disease.

2. Possible Causes of ADHD

Although many theories have been investigated, the cause of ADHD remains a mystery. None of the results of the experiments have led to a clear and compelling outcome. A nutritional deficiency of some sort remains high on the list of candidate causes (Dietary Theories for ADHD) . Potential deficiencies in several different vitamins and rare metals, such as zinc, magnesium, iron, and vitamin B6 have been posited, but in controlled studies, supplements have failed to show statistically significant improvements. The fact that ADHD appears to be especially prevalent in America suggests that it has something to do with differences between the American diet and the diet of other countries. To me, the most obvious difference is America's obsession with low fat diet. Today it is practically impossible to find full-fat yogurt at an American grocery store, and non-fat or low-fat products crowd out the full-fat versions of the same things on grocery shelves. Marketing ploys are proud to boast that a given product contains little, or, better yet, no, fat.

The nutritional theory for ADHD that has gained the most traction is that it may be caused by a deficiency or imbalance in essential fatty acids. These are omega-3 and omega-6 fats, which are widely available in meats, fish, and eggs. Humans are unable to manufacture these fats naturally from other dietary sources. While omega-6 fats are also found in vegetable oil, omega-3 fats are only abundant in animal fat, especially cold-water fish. Experiments that provide ADHD children with an omega-3 supplement have shown modest but encouraging results. However, I'm not proposing simply adding an omega-3 pill alongside the Ritalin tablet. I'm proposing that the cheerios and skim milk for breakfast be replaced with bacon and eggs; that the diet coke for lunch be replaced with whole milk, and the lean turkey breast in the sandwich be replaced with dark tuna, peanut butter, or liverwurst (a healthy choice that has all but disappeared from America's grocery shelves).

Another theory suggests that ADHD may be due to too much dietary refined sugar [16]. This theory also makes sense because the near absence of fat, coupled with an overabundance of high glycemic index foods, leads to a wildly unstable food supply in the blood. Glucose levels in the blood skyrocket immediately after a meal, and this triggers a sharp increase in insulin supply, rushed out by the pancreas to process the glucose. However, as long as the insulin concentration in the blood is high, fats that are stored in fat cells remain inaccessible and are not released into the blood. Many of the body's cells can utilize either glucose or fats as fuel. However, the brain can not utilize fats for fuel, but, critically, needs fat as raw material for construction of its network of nerve fibers. This is especially true for a growing child with a maturing brain. The brain needs a simultaneous presence of adequate glucose and adequate fat, something that is very hard to achieve when fats are unavailable from food sources, and high glycemic index foods are abundant.

Previous experiments conducted to test whether too much sugar causes ADHD involve substituting aspartame (a zero-calorie sweetener) for sugar [32]. I am not surprised that these experiments have failed, because aspartame is arguably even more damaging than sugar: the sweet taste on the tongue triggers the release of insulin, but there is no sugar for the insulin to break down. Hence the insulin lingers longer in the blood and fat release from available stores is further suppressed.

There is a strong genetic component to ADHD, i.e., it tends to run in families [8]. But this does not mean that the cause is genetic. Instead, genetic factors predispose individuals to develop alternative strategies for coping with nutritional deficiencies, that lead to different, but perhaps equally damaging, health issues. I would argue that, in the case of ADHD, genetics determine how the body manages homeostasis in the face of excess carbohydrates along with dietary deficiencies in essential fatty acids. (With respect to nutrition, homeostasis refers to the maintenance of a stable supply of glucose and fatty acids in the blood under varying conditions of food supply.) Studies to determine which genes are involved in ADHD have turned up hundreds of genes that play a role, but each gene has only a very small influence, so the relationship to genetics is extremely complex.

3. My Theory for the Cause of ADHD

It appears to me that at least two complementary coping mechanisms have been developed in different segments of the population to adjust metabolism for dietary fat deficiency. One coping mechanism, which I described in my essay on obesity, involves storing a steadily expanding "silo" of fat reserves on the body. The alternative mechanism, which I now believe is the one adopted by children with ADHD, is to implement a fat conservation mode: to manipulate the body's energy requirements towards favoring glucose over fat, while simultaneously stunting growth and compromising brain development.

While in my essay on obesity I argued that the obese suffer from defective glucose metabolism in the muscles, it appears that children with ADHD suffer from the exact opposite problem: very efficient glucose metabolism. Insulin is critical for the metabolism of glucose. When insulin levels are high, body fat cells are unable to release their fat stores, as shown in the figure at the right [lipolysis = breakdown of fat tissue]. I have proposed that obesity is protective against ADHD because the abundant fat cells can release plenty of triglycerides into the blood early in the morning, before the first meal. This fat supply can tide the person over through the long fatty-acid drought that occurs during the day, while an abundance of high-glycemic index low-fat foods are consumed. A further advantage is that obese people typically have reduced insulin production (due to insufficient calcium, which I explain later), so the levels of insulin in the blood are never excessively high. Their muscle cells have been programmed to prefer fat metabolism, but there is also plenty of fat available from the triglycerides (released before the meal began) to supply the brain's raw materials to enhance communication through neural pathways. Furthermore, the glucose that is not consumed by the muscles is readily available

It seems that ADHD children have adopted an entirely different strategy for coping with insufficient fats in the food sources. Research has shown that many of them suffer from hypoglycemia (low blood sugar), because their insulin is extremely efficient -- the opposite of diabetes [19]. In direct contrast with obese people, the fat cells of ADHD children program the muscles to prefer glucose over fat as a fuel source. This reduces the burden placed on the fat cells to convert glucose to fat, which is a very inefficient process. Furthermore, unlike the obese, ADHD children typically have no shortage of insulin, produced by the pancreas in response to glucose. Insulin enables the muscles to readily consume the glucose, but also unfortunately supresses the ability of the fat cells and the liver to release stored fats. If there is plenty of glucose in the consumed foods, and very little fat, then the muscles and brain consume the glucose, but the brain is deprived of sufficient fats to construct high quality long-distance neural connections. ADHD children have been found to have shrunken white matter in parts of the brain that are involved with focus of attention and learning new knowledge. I believe this is a direct consequence of a lack of a supply of fats, critically, when the neural pathways that make up the white matter are actively being formed.

The body with inadequate fat supply in the food sources is essentially like a car engine running on only two cylinders. While it has been argued that the body can manufacture all the fats it needs from other sources such as glucose, this is not actually true. The body uses fats not only as an energy source, but also, crucially, as a component of cell walls and as the insulation that covers all nerve fibers, i.e., the myelin sheath, not just in the brain but everywhere in the body. Two specific kinds of fats, omega-3 fats and omega-6 fats, are called "essential fatty acids" (EFA's) because the body cannot manufacture them. It is essential to obtain them from food sources such as meat, eggs, and fish.

Furthermore, the body cannot produce fat supply in the blood stream "at will." As I have mentioned previously, when insulin levels are high, the subcutaneous fat cells and the abdominal fat cells, as well as the liver, are suppressed from releasing their stored fats. When glucose is available, the fat cells are otherwise engaged in the task of taking up the glucose and converting it into additional fat supplies. The presence of insulin disables the process of lipolysis that is necessary before the stored fats can be released into the blood stream.

4. Nutritional Deficiency and ADHD

A husband and wife team of nutrition experts, Fred and Alice Ottoboni, have published an excellent article on the theory that ADHD might be a nutritional deficiency disease [25]. They draw analogies with Beriberi and Pellagra which became endemic in previous centuries as a consequence of significant dietary changes within a large population. The wholesale switch from brown to white rice in Asia in the 1800's led to many deaths from Beriberi, and the switch from meat, eggs, and milk to corn led to widespread Pellagra in western nations at the same time.

They argue that ADHD may be a direct consequence of a large shift in dietary practices that has taken place in America over the last 40 years -- a shift towards increased consumption of processed foods containing an overabundance of sugar and starch, along with a dramatic shift in the sources of fat from meat, fish, and eggs to vegetable fats and oils. They express concern about both the high ratio of omega-6 to omega-3 fats (20:1) in vegetable oils, as well as their propensity to become highly damaging trans fats if overheated. They specifically mention the importance of DHA (docosahexaenic acid), found in meats and eggs, and AA (arachidonic acid), found in cold water fish.

These authors cite a number of different studies that have shown a relationship between fatty acid deficiency and ADHD [15] [34] or a decrease in brain size in ADHD children [22] [26]. They also suggest that the observed difference in IQ between breast fed and bottle fed infants may be due to the higher concentration of DHA and AA in breast milk. This deficiency is now fortunately being aggressively corrected both in America and elsewhere in the world (Recommendations for AA and DHA in Baby Formula) , and we can hope that this will lead to a decrease in the incidence of ADHD looking forward.

A study by Price on the health of isolated racial groups compared those who remained on their indigenous diet with those who transitioned to a western diet [26]. The indigenous diet invariably contained essentially no empty carbs, and included large amounts of meat and fish. The children who switched to the "modern" diet showed symptoms of both physical and mental degeneration.

Ottoboni and Ottoboni conclude with this rather ominous remark: "The choice seems clear. We can either continue to depend on prescription drugs to mask the symptoms of ADHD, or consider preventing ADHD by modifying the American diet, particularly for child bearing women and children. Should we decide to continue to depend on prescription drugs, which do not remedy the underlying causes of nutritional deficiency diseases, we can look forward to a country in which there will be more and more children with undersized brains who cannot learn, use costly prescription drugs, drop out of school, commit crimes, and cause anguish for their parents."

5. Fats and the Brain

Children are especially vulnerable to inadequate fat suppply due to their rapidly developing brain. The brain does not consume fat as fuel -- this would be problematic because it would lead to a cannibalistic behavior where the brain would feed off of itself. According to the Franklin Institute, as much as two-thirds of the brain's mass consists of fats. The membranes of neurons consist of a thin double layer of fatty acid molecules. The myelin sheath that encases each fiber in the network of nerve fibers that make up the "white matter" consists of 70% fat and 30% protein. A child's brain is constantly laying down new connections and reshaping old connections to incorporate new experiences and knowledge into long term memory. This processing requires a steady and reliable supply of fats.



Through a technique known as "diffusion tensor imaging" (DTI), scientists have been able to examine the brains of children with and without a diagnosis of ADHD (Brain Differences in ADHD) [5]. They found several differences, most notably, in the volume of white matter connecting together the frontal cortex, basal ganglia, brainstem, and cerebellum. These areas are involved in higher level thought and reasoning, attention, impulsive behaviour, inhibition, and motor activity. Never-medicated ADHD children had noticeably smaller volume of white matter in these areas, compared to normal children or to ADHD children who had been treated with medications such as Ritalin.

White matter consists of a massively interconnected network of nerve fibers, each of which is coated with a fatty myelin sheath that keeps the message insulated (i.e, keeps the signal strong) and greatly increases the transmission speed. In order to focus attention, the brain releases the hormone dopamine from centers in the midbrain, and dopamine receptors transmit signals over long distance pathways to the frontal cortex, the basal ganglia, and the cerebellum, as shown in the figure on the left. Dopamine is a crucial hormone that orchestrates the brain's thought processes involved in maintaining attention to a task and subsequently acquiring new knowledge. Defective dopamine utilization is widely suspected to play a role in ADHD [36]. Poor quality white matter on these long-distance connections, as a consequence of insufficient supply of fat from the blood, would have a huge impact on the ability to pay attention and to learn new facts.

A very exciting research direction that has been undertaken recently addresses the question of the rate of maturation of the brain [31]. 223 children with ADHD were compared with 223 non-ADHD controls. The research utilized magnetic resonance scans to estimate the thickness of the cerebral cortex at more than 40,000 sample points at different positions along the brain surface. Typically, the thickness increases during childhood and then decreases during adolescence. From samples taken over a period of several years, researchers can pinpoint the point in time when the cortex is thickest. The results of the experiments were remarkable: children with ADHD reached peak thickness much later (on average at 10 and a half years old) than children without ADHD (on average at 7 and a half years old). The biggest delay showed up in regions of the prefrontal cortex (shown in the figure on the right) that control attention and motor planning.

Such a delay in maturation would be a good conservation strategy if there is insufficient fat in the diet. By slowing down the growth rate of the cortex, less demand is placed to acquire adequate fat supply, needed to grow additional neurons and myelinated nerve fibers. The body's stunted growth (another characteristic of ADHD children) could even be a side effect of the need to delay the rate of maturation of the brain. Decreasing the concentration of growth hormone would likely affect both the brain and the body, leading to a consistent slowing down of maturation rates across the board.

6. Managing Homeostasis without Dietary Fats

Fats are a much more stable energy source than carbohydrates. Sugars and starches, especially in the form of high glycemic index "empty carbs," are absorbed very quickly into the blood stream, causing a sharp spike in the glucose level. This in turn triggers the pancreas to inject a large amount of insulin into the blood, to promote the uptake of the glucose into the body's cells. Carbohydrates ingested without fats are absorbed much more rapidly than carbohydrates buffered by fat, because fat slows down the digestive process. Fats, being digested much more slowly, will become available as an alternative fuel source just as the carbohydrate supplies are becoming exhausted. But this is true only if sufficient fats are consumed with the meal.

Very little excess glucose can be stored in the body for later use, unless it is first converted to fat. The liver can provide a small buffer of glucose stored in the form of glycogen, amounting to no more than 5% of its total mass. Once that capacity is exceeded, any remaining glucose in the blood must be converted to fat to be stored.

A thin child whose diet consists mainly of empty carbs cycles between feast and famine in terms of glucose supply, but suffers chronically from an inadequate supply of fats. This places a lot of stress on the homeostasis system because of the gross imbalance between glucose and fat in the external fuel supply. A solution to this problem can be achieved by piling fat stores on the body, except that the fat stores themselves introduce additional energy needs and the strategy snowballs into obesity.

For the ADHD person, instead of steadily accumulating fat stores and programming the muscles to preferentially consume fats, I argue that their bodies have adopted a strategy of fat conservation. The muscles are programmed to prefer glucose over fat, and the body size is minimized by reducing fat deposits, slowing down the maturation process, and stunting growth. As a consequence of the body's reduced needs for fats, more fat (but still not enough) is available to the brain to support its need to build myelin sheath for the expanding network of nerve fibers.