Saturday, November 21, 2009
13. ADHD and Sleep Disorders
A recent study has shown that adolescents diagnosed with ADHD are significantly more likely to suffer from sleep disorders such as insomnia, sleep terrors, nightmares, and snoring, compared to controls. I suspect these problems during sleep stem from insufficent fats. The brain is unable to properly integrate the newly acquired knowledge and experiences of the day before into long term memory stores, due to the insufficient supply of fats to build the myelin sheaths surrounding newly constructed nerve fibers and reinforcements. These deficiencies in resources critical to the goals of sleeping may be the source of extreme restlessness, wakefulness, and night terrors.
14. The Beneficial Effects of Hyperactivity
One of the well-known characteristics of ADHD children is that they are fidgety. Whenever they are trying hard to concentrate, they are in constant motion, unable to sit still, and it has been hypothesized that such kinesthetics
actually help them think. One way random movements could be effective is through activating dopamine release. Dopamine plays a critical role in body movement: people with Parkinson's disease are unable to initiate movement and appear paralyzed unless treated with the dopamine precursor, L-dopa. I hypothesize that, through random movements of their limbs, ADHD children are able to stimulate the release of dopamine, and thus increase its bioavailability for the important other roles involved in attention and learning.
A further benefit of the random movements is that they involve anaerobic metabolism of glucose, which consumes the glucose stores in the muscles and releases lactic acid into the blood stream. While lactic acid had been generally considered to be a waste product, it has recently been discovered, quite remarkably, that the heart is able to metabolize lactic acid directly as an alternative source of fuel [6]. This has the effect of sparing fatty acids that the heart would otherwise consume. Furthermore, and, most surprisingly, the brain can also utilize lactate as a fuel source [27]. The brain's consumption of glucose falls substantially after extended anaerobic exercise, since it can also exploit the lactic acid that builds up in the blood as a by-product of anaerobic glucose metabolism.
Thirdly, the depletion of glucose in the muscles is followed by replenishment of the muscles' private stores, which will use up insulin in the process. This accomplishes the important goal of driving down the insulin levels so that the fat cells and liver can release more fats into the blood.
Finally, and perhaps most importantly, exercise stimulates the release of adrenaline from the sympathetic nervous system, and adrenaline is the most significant hormone for allowing fat release from the fat cells, even in the presence of excess insulin [24].
Thus, all of these contributions, the production of lactic acid which can be used by the heart for fuel, the depletion of insulin, and the activation of adrenaline, which will actively promote the release of fats, will contribute towards the goal of increasing the fat supply available for the brain.
actually help them think. One way random movements could be effective is through activating dopamine release. Dopamine plays a critical role in body movement: people with Parkinson's disease are unable to initiate movement and appear paralyzed unless treated with the dopamine precursor, L-dopa. I hypothesize that, through random movements of their limbs, ADHD children are able to stimulate the release of dopamine, and thus increase its bioavailability for the important other roles involved in attention and learning. A further benefit of the random movements is that they involve anaerobic metabolism of glucose, which consumes the glucose stores in the muscles and releases lactic acid into the blood stream. While lactic acid had been generally considered to be a waste product, it has recently been discovered, quite remarkably, that the heart is able to metabolize lactic acid directly as an alternative source of fuel [6]. This has the effect of sparing fatty acids that the heart would otherwise consume. Furthermore, and, most surprisingly, the brain can also utilize lactate as a fuel source [27]. The brain's consumption of glucose falls substantially after extended anaerobic exercise, since it can also exploit the lactic acid that builds up in the blood as a by-product of anaerobic glucose metabolism.
Thirdly, the depletion of glucose in the muscles is followed by replenishment of the muscles' private stores, which will use up insulin in the process. This accomplishes the important goal of driving down the insulin levels so that the fat cells and liver can release more fats into the blood.
Finally, and perhaps most importantly, exercise stimulates the release of adrenaline from the sympathetic nervous system, and adrenaline is the most significant hormone for allowing fat release from the fat cells, even in the presence of excess insulin [24].
Thus, all of these contributions, the production of lactic acid which can be used by the heart for fuel, the depletion of insulin, and the activation of adrenaline, which will actively promote the release of fats, will contribute towards the goal of increasing the fat supply available for the brain.
15. How Ritalin Works
In the United States, a popular drug to treat ADHD is Ritalin. It is estimated that as many as 10% of the children in the U.S. now take Ritalin or another stimulant [3], and the U.S. consumes 90% of the Ritalin being manufactured worldwide. Since ADHD children suffer from a reduced number of dopamine receptors in the brain [36], it is hypothesized that Ritalin is effective because it prevents the reuptake of dopamine and allows it to stay in the intercellular spaces for a substantially longer time.
Ritalin has a calming effect on ADHD children. This is understandable since Ritalin both increases the bioavailability of dopamine and suppresses insulin's ability to block fat release from storage sites; i.e., it accomplishes the same two goals that random movements try to accomplish. However, children on Ritalin complain that it results in an initial burst of energy with a racing heart, followed by a period of physical exhaustion ([3], p. 112). The energy burst is associated with the adrenaline rush, and the exhaustion is likely a consequence of depleted supplies of both fats and glucose, once the Ritalin has worn off.
Dopamine is a precursor to adrenaline, the "fight or flight" hormone. If dopamine is allowed to linger longer in a bioavailable state through the action of Ritalin, then adrenaline levels will go up. Adrenaline is a very powerful hormone with diverse effects on the body, mainly aimed at increasing fuel supply to the blood in the short term, i.e., to operate in crisis mode.
One crucial effect adrenaline has is to disable insulin's suppressive effect on the fat cells [24]. This allows them to release their fats even while insulin levels are high. Ritalin thus enables the brain to be simultaneously well supplied with glucose for fuel, fat for nerve fiber construction, and dopamine to control execution of the focus and memory consolidation tasks involved with learning new knowledge.
Through its effect of increasing adrenaline levels, Ritalin also suppresses appetite. In the "fight or flight" reaction, the digestive system is shut down, in order to conserve energy, since the digestion process itself consumes energy. Nearly all ADHD children on Ritalin lose weight, and many become dangerously thin over time. A positive effect of reduced appetite is that it likely leads to an increase in the bias towards glucose consumption and fat conservation, as I argued in the section on anorexia. However, in the long term, the depleted fat reserves eventually further aggravate the original problem of insufficient fat supply.
Ritalin has a calming effect on ADHD children. This is understandable since Ritalin both increases the bioavailability of dopamine and suppresses insulin's ability to block fat release from storage sites; i.e., it accomplishes the same two goals that random movements try to accomplish. However, children on Ritalin complain that it results in an initial burst of energy with a racing heart, followed by a period of physical exhaustion ([3], p. 112). The energy burst is associated with the adrenaline rush, and the exhaustion is likely a consequence of depleted supplies of both fats and glucose, once the Ritalin has worn off.
Dopamine is a precursor to adrenaline, the "fight or flight" hormone. If dopamine is allowed to linger longer in a bioavailable state through the action of Ritalin, then adrenaline levels will go up. Adrenaline is a very powerful hormone with diverse effects on the body, mainly aimed at increasing fuel supply to the blood in the short term, i.e., to operate in crisis mode.
One crucial effect adrenaline has is to disable insulin's suppressive effect on the fat cells [24]. This allows them to release their fats even while insulin levels are high. Ritalin thus enables the brain to be simultaneously well supplied with glucose for fuel, fat for nerve fiber construction, and dopamine to control execution of the focus and memory consolidation tasks involved with learning new knowledge.
Through its effect of increasing adrenaline levels, Ritalin also suppresses appetite. In the "fight or flight" reaction, the digestive system is shut down, in order to conserve energy, since the digestion process itself consumes energy. Nearly all ADHD children on Ritalin lose weight, and many become dangerously thin over time. A positive effect of reduced appetite is that it likely leads to an increase in the bias towards glucose consumption and fat conservation, as I argued in the section on anorexia. However, in the long term, the depleted fat reserves eventually further aggravate the original problem of insufficient fat supply.
16. The Dangers of Ritalin Use
It seems to be remarkably easy to pursuade most Americans that popping a designer pill is the answer to nearly all problems. There is great irony, however, in the fact that many children in America are told, on the one hand, to "say 'no' to drugs," and then, on the other hand, to take a drug which is in many ways equivalent to amphetamines like speed and cocaine. Increasingly, friends of ADHD children are obtaining the drug and then snorting it or shooting it like cocaine to achieve an intense high (Ritalin Abuse). And the children are often naive about the dangers of Ritalin, thinking that, if doctors prescribe it for young children, it must be harmless.
Dr. Peter Breggin has become a strong advocate of the idea that widespread Ritalin use in America is causing far more harm than good. His book, Talking back to Ritalin, [3] presents a compelling argument that, despite the assurances from doctors that it is a safe
drug, Ritalin is a very close cousin to amphetamines and exhibitis all of the same dangerous properties leading to addiction and abuse. He cites a 1998 study [18] which showed that the use of a childhood stimulant such as Ritalin "is significantly and pervasively implicated in the uptake of regular smoking, in daily smoking in adulthood, in cocaine dependence, and in lifetime use of cocaine and stimulants."
He also points out that Ritalin is classed with amphetamines in terms of its clinical effects. Ritalin is labelled "Schedule II" by both the DEA and the International Narcotics Control Board. Schedule II for a prescription drug indicates the highest possible potential for abuse. A study comparing Ritalin with cocaine claimed that "Methylphenidate [Ritalin], like cocaine, increases synaptic dopamine by inhibiting dopamine reuptake, it has equivalent reinforcing effects to those of cocaine, and its intravenous administration produces a 'high' similar to that of cocaine" [37].
Aside from its potential for abuse, and its potential to lead to abuse of other drugs later in life, long term Ritalin use, as prescribed, leads to several other adverse health issues. The shutting down of the digestive system suppresses appetite, with subsequent weight loss and stunted growth. By simulating a "fight or flight" reaction, it increases both blood pressure and heart rate [1], and may do other unknown damage to the heart. In March, 2000, a 14-year old boy, Matthew Smith, fell off his skate board and died suddenly. A subsequent autopsy showed severe heart damage, which the coroner suspected was due to the fact that he had been taking Ritalin since he was six years old. This has stirred up considerable discussion among parents of ADHD children regarding the safety of long-term Ritalin use (Matthew Smith Ritalin Discussion). Parents are now urged to screen their children for possible heart conditions if they are considering Ritalin as a treatment option.
More ominously, by overworking the dopamine system, long term Ritalin use may lead to Parkinson's disease much later in life. It has been demonstrated that other drugs that affect the dopamine system can cause Parkinson's disease. Through population studies, amphetamine use many years before was correlated with Parkinson's disease much later in life [10]. Adderall, another popular drug for treating ADHD, is an amphetamine, and Ritalin is a close cousin. In 1983, a defective batch of the street drug, synthetic heroin, also known as "China White", hit the streets of San Francisco, and a number of addicts who were unfortunate victims of this mistake acquired severe irreversible Parkinson's disease after just a single dose, due to the neurotoxin MPTP inadvertently present in the drug. While such a dramatic instantaneous effect would not be expected to occur with Ritalin, it is impossible to predict what will happen long term. I hope I am wrong, but I believe it is likely that we will see a substantial increase in the incidence of Parkinson's disease later in life among today's Ritalin and Adderall users.
Dr. Peter Breggin has become a strong advocate of the idea that widespread Ritalin use in America is causing far more harm than good. His book, Talking back to Ritalin, [3] presents a compelling argument that, despite the assurances from doctors that it is a safe
drug, Ritalin is a very close cousin to amphetamines and exhibitis all of the same dangerous properties leading to addiction and abuse. He cites a 1998 study [18] which showed that the use of a childhood stimulant such as Ritalin "is significantly and pervasively implicated in the uptake of regular smoking, in daily smoking in adulthood, in cocaine dependence, and in lifetime use of cocaine and stimulants."He also points out that Ritalin is classed with amphetamines in terms of its clinical effects. Ritalin is labelled "Schedule II" by both the DEA and the International Narcotics Control Board. Schedule II for a prescription drug indicates the highest possible potential for abuse. A study comparing Ritalin with cocaine claimed that "Methylphenidate [Ritalin], like cocaine, increases synaptic dopamine by inhibiting dopamine reuptake, it has equivalent reinforcing effects to those of cocaine, and its intravenous administration produces a 'high' similar to that of cocaine" [37].
Aside from its potential for abuse, and its potential to lead to abuse of other drugs later in life, long term Ritalin use, as prescribed, leads to several other adverse health issues. The shutting down of the digestive system suppresses appetite, with subsequent weight loss and stunted growth. By simulating a "fight or flight" reaction, it increases both blood pressure and heart rate [1], and may do other unknown damage to the heart. In March, 2000, a 14-year old boy, Matthew Smith, fell off his skate board and died suddenly. A subsequent autopsy showed severe heart damage, which the coroner suspected was due to the fact that he had been taking Ritalin since he was six years old. This has stirred up considerable discussion among parents of ADHD children regarding the safety of long-term Ritalin use (Matthew Smith Ritalin Discussion). Parents are now urged to screen their children for possible heart conditions if they are considering Ritalin as a treatment option.
More ominously, by overworking the dopamine system, long term Ritalin use may lead to Parkinson's disease much later in life. It has been demonstrated that other drugs that affect the dopamine system can cause Parkinson's disease. Through population studies, amphetamine use many years before was correlated with Parkinson's disease much later in life [10]. Adderall, another popular drug for treating ADHD, is an amphetamine, and Ritalin is a close cousin. In 1983, a defective batch of the street drug, synthetic heroin, also known as "China White", hit the streets of San Francisco, and a number of addicts who were unfortunate victims of this mistake acquired severe irreversible Parkinson's disease after just a single dose, due to the neurotoxin MPTP inadvertently present in the drug. While such a dramatic instantaneous effect would not be expected to occur with Ritalin, it is impossible to predict what will happen long term. I hope I am wrong, but I believe it is likely that we will see a substantial increase in the incidence of Parkinson's disease later in life among today's Ritalin and Adderall users.
17. My Recommendations for Treating ADHD
In this section, I will present my own ideas on how children with ADHD can, with time, improve their brain function and reduce their dependence on Ritalin. First of all, I want to remind you that I am not an M.D. My doctorate from MIT is in electrical engineering. However, my PhD thesis concerned an auditory model for human speech processing, and thus required extensive reading on neural mechanisms in the brain. My Bachelor's degree from MIT is in biology, with a minor in food and nutrition. I benefit strongly from having been exposed to ideas about nutrition before the low-fat diet craze got its firm grip on our nation's population.
The first step towards healing is to discard the idea that fats are unhealthy. I recommend reading any of the following books, which have covered the subject extensively, Good Calories Bad Calories by the New York Times reporter, Gary Taubes [35], Fat and Cholesterol are Good For You, by Uffe Ravnskov, a Swedish M.D., Ph.D. [28], and Trick and Treat: How 'Healthy Eating' is Making us Ill, by the British researcher and writer, Barry Groves [11].
We have been led by the American medical community to believe that a high-fat diet leads to heart disease, and that increased dietary consumption of fruits and vegetables is a heart-healthy choice. However, a recent (2009) long-term population-based study in Sweden has concluded that fruits and vegetables provide no heart-health benefit at all unless they are consistently eaten with fats [14]. The researchers conducted extensive interviews with several thousand men in rural Sweden about their food practices, and also carefully monitored their heart health status over a 12-year period. Surprisingly, they found no association between coronary disease and the consumption of fish or wholemeal bread, and no association with the consumption of fruits and vegetables, for those who also chose low fat dairy, or consumed little dairy. The only clear benefit they could find was with a combination of lots of fruits and vegetables and high-fat dairy consumption. They hypothesized that the high fat dairy was required to promote the absorption of the vitamins and minerals contained in the fruits and vegetables. However, if they are eating both lots of fat and lots of fruits and vegetables, they are probably also eating few empty carbs. A corollary of this result is that a person who avoids fat is likely deficient in vitamins and minerals, even if they consume a lot of fruits and vegetables.
Once a mother no longer fears fats, she can begin to change her child's diet, with the goal of over-correcting the fatty acid deficit through a high fat, very low carb, diet. An increase in the consumption of meat, fish, and eggs should be balanced with a decrease in the consumption of sugar and starch. Foods containing trans fats should be carefully avoided. Improvements will probably not be dramatic, as it will take a long time for the child to repair all the poorly insulated nerve fibers that are suffering from insufficient fat supply. I can not predict how quickly or how completely a child who has suffered from dietary fat deficiency throughout its life can recover, once the dietary correction is in place.
Of course, the best action would be to avoid the problem in the first place, and this begins with the pregnant mother. It is especially important for her to consume an abundance of omega-3 and omega-6 fats while she is carrying the baby, and to continue to do so once the baby is born, to assure a high-quality milk supply to her child. A recent analysis of data from the Nurses' Health Study, an ambitious long-term study involving over 18,000 nurses, showed that fat in dairy consumption was associated with high fertility. Women who said they ate low-fat diary increased their risk of infertility by 85%, whereas women who consistently ate high-fat dairy decreased their risk by 27% [7]. Fertility is an indicator of the degree to which the body perceives that it is prepared to support a fetus. Breast milk has an extremely high fat content, significantly higher than that of cow's milk. It then seems logical that, once mother's milk is replaced with table foods, these foods should continue to be high in fat content.
I find Ritalin to be a very disturbing drug, particularly because it is a synthetic drug and because it has been on the market for a relatively short time. We have no idea what will happen to children currently taking Ritalin 40 or 50 years hence. Alarm bells have already been raised regarding possible addiction and abuse, appetite loss and subsequent malnutrition and stunted growth, and adverse effects to the heart.
Other stimulants that occur in nature have been used by humans for hundreds of years, and they would likely be safer than Ritalin if they can achieve the same goals. I am thinking of caffeine, chocolate, and even nicotine. It's possible that nicotine is no better than Ritalin, with its known issues regarding the potential for addiction and increased risk for heart disease and lung cancer. But a nicotine patch, which avoids the issue of tar exposure in the lungs leading to lung cancer, is at least an alternative that should be considered instead of Ritalin.
Coffee is a particularly attractive choice -- it has been extremely well studied and appears to have very few if any adverse side effects. It has been shown to improve memory, and it works in part because, in addition to increasing adrenaline levels, it acts directly to disable insulin's suppression of fat release [23], which I consider to be one of the most important goals of an ADHD drug. Chocolate is a stimulant that children will find especially appealing, and chocolate milk (made from whole milk) would be a great way to introduce it.
The first step towards healing is to discard the idea that fats are unhealthy. I recommend reading any of the following books, which have covered the subject extensively, Good Calories Bad Calories by the New York Times reporter, Gary Taubes [35], Fat and Cholesterol are Good For You, by Uffe Ravnskov, a Swedish M.D., Ph.D. [28], and Trick and Treat: How 'Healthy Eating' is Making us Ill, by the British researcher and writer, Barry Groves [11].
We have been led by the American medical community to believe that a high-fat diet leads to heart disease, and that increased dietary consumption of fruits and vegetables is a heart-healthy choice. However, a recent (2009) long-term population-based study in Sweden has concluded that fruits and vegetables provide no heart-health benefit at all unless they are consistently eaten with fats [14]. The researchers conducted extensive interviews with several thousand men in rural Sweden about their food practices, and also carefully monitored their heart health status over a 12-year period. Surprisingly, they found no association between coronary disease and the consumption of fish or wholemeal bread, and no association with the consumption of fruits and vegetables, for those who also chose low fat dairy, or consumed little dairy. The only clear benefit they could find was with a combination of lots of fruits and vegetables and high-fat dairy consumption. They hypothesized that the high fat dairy was required to promote the absorption of the vitamins and minerals contained in the fruits and vegetables. However, if they are eating both lots of fat and lots of fruits and vegetables, they are probably also eating few empty carbs. A corollary of this result is that a person who avoids fat is likely deficient in vitamins and minerals, even if they consume a lot of fruits and vegetables.
Once a mother no longer fears fats, she can begin to change her child's diet, with the goal of over-correcting the fatty acid deficit through a high fat, very low carb, diet. An increase in the consumption of meat, fish, and eggs should be balanced with a decrease in the consumption of sugar and starch. Foods containing trans fats should be carefully avoided. Improvements will probably not be dramatic, as it will take a long time for the child to repair all the poorly insulated nerve fibers that are suffering from insufficient fat supply. I can not predict how quickly or how completely a child who has suffered from dietary fat deficiency throughout its life can recover, once the dietary correction is in place.
Of course, the best action would be to avoid the problem in the first place, and this begins with the pregnant mother. It is especially important for her to consume an abundance of omega-3 and omega-6 fats while she is carrying the baby, and to continue to do so once the baby is born, to assure a high-quality milk supply to her child. A recent analysis of data from the Nurses' Health Study, an ambitious long-term study involving over 18,000 nurses, showed that fat in dairy consumption was associated with high fertility. Women who said they ate low-fat diary increased their risk of infertility by 85%, whereas women who consistently ate high-fat dairy decreased their risk by 27% [7]. Fertility is an indicator of the degree to which the body perceives that it is prepared to support a fetus. Breast milk has an extremely high fat content, significantly higher than that of cow's milk. It then seems logical that, once mother's milk is replaced with table foods, these foods should continue to be high in fat content.
I find Ritalin to be a very disturbing drug, particularly because it is a synthetic drug and because it has been on the market for a relatively short time. We have no idea what will happen to children currently taking Ritalin 40 or 50 years hence. Alarm bells have already been raised regarding possible addiction and abuse, appetite loss and subsequent malnutrition and stunted growth, and adverse effects to the heart.
Other stimulants that occur in nature have been used by humans for hundreds of years, and they would likely be safer than Ritalin if they can achieve the same goals. I am thinking of caffeine, chocolate, and even nicotine. It's possible that nicotine is no better than Ritalin, with its known issues regarding the potential for addiction and increased risk for heart disease and lung cancer. But a nicotine patch, which avoids the issue of tar exposure in the lungs leading to lung cancer, is at least an alternative that should be considered instead of Ritalin.
Coffee is a particularly attractive choice -- it has been extremely well studied and appears to have very few if any adverse side effects. It has been shown to improve memory, and it works in part because, in addition to increasing adrenaline levels, it acts directly to disable insulin's suppression of fat release [23], which I consider to be one of the most important goals of an ADHD drug. Chocolate is a stimulant that children will find especially appealing, and chocolate milk (made from whole milk) would be a great way to introduce it.
18. ADHD: Conclusion
ADHD is a syndrome manifested mainly by hyperactivity and inattentiveness. It affects as many as 10% of boys in the U.S., and perhaps 3% of girls. Children are usually diagnosed during the first few years in school, although it is often believed that they have suffered from the condition since birth. Increasingly, treatment involves a prescription of Ritalin, a drug that has been shown to be effective in calming them down and improving attention span, often leading to higher grades at school. The syndrome was not even listed in the first edition of the DSM (Diagnostic and Statistical Manual of Mental Disorders) issued in 1968, but appeared in the second edition, released in 1980. During the intervening period, the message that dietary fats are harmful to health first made its appearance [17].
I agree with Peter Breggin when he claims in his book Talking back to Ritalin that long term Ritalin use will likely lead to many dire consequences down the road. However, he also claims that ADHD is a fake disease, concocted purely to stuff the pockets of the pharmaceutical industry executives. I try to imagine what it would be like to be a parent of an ADHD child, reading that ADHD is caused purely by social influences -- that the inattentiveness and hyperactivity are due to a dysfunctional family life and/or an unstimulating school environment. I am reminded of the time when autism was blamed on poor parenting. A mother who has done everything she can to create a nurturing environment but has seen no improvement in her child's symptoms must feel very besieged, frustrated, and discouraged.
I believe that ADHD is a real syndrome with a strong genetic component. However, I have argued that the genetic aspect is manifested as a greater susceptibility to brain dysfunction as a consequence of insufficient fats in the diet. This includes the diet of both the child and the mother while she carried the child to term, and while she nursed the child. I believe that symptoms will improve slowly over time if the child's diet is simply adjusted to include more meats, eggs, fish, and high-fat dairy, while minimizing the consumption of empty carbs.
Unfortunately, I doubt that the symptoms will ever go away entirely, especially if the child is already a teenager by the time the change is implemented. I do not know how much of the damage in neural connections in the brain and nervous system can be repaired long after critical developmental milestones have passed. However, children's brains have been shown to be remarkably resilient after brain injury, so we can hope that significant improvement can take place over time. Of course "an ounce of prevention is worth a pound of cure." Anyone who is thinking of starting a family would be wise to change their diet in anticipation of the coming pregnancy -- to stop worrying about the mistaken belief that animal fats are unhealthy, and switch to high-fat dairy, meats, fish, and eggs instead of sugar-laden drinks and starchy foods.
I find it impossible to blame the mother for the problem -- she is only executing on both subliminal and overt messages claiming that dietary fat is unhealthy and will lead to obesity and heart disease. She is trying her best to provide her child with a healthy diet according to strong advice from both the U.S. government and the American medical establishment. I therefore expect ADHD to persist unabated in the U.S. until the authoritarian figures finally recognize and acknowledge their error, and change their tune regarding dietary fat. It is very disturbing to think of how many years it may take for them to own up to the huge mistake they have made by advocating low-fat diet, and the enormous anguish it has caused.
I agree with Peter Breggin when he claims in his book Talking back to Ritalin that long term Ritalin use will likely lead to many dire consequences down the road. However, he also claims that ADHD is a fake disease, concocted purely to stuff the pockets of the pharmaceutical industry executives. I try to imagine what it would be like to be a parent of an ADHD child, reading that ADHD is caused purely by social influences -- that the inattentiveness and hyperactivity are due to a dysfunctional family life and/or an unstimulating school environment. I am reminded of the time when autism was blamed on poor parenting. A mother who has done everything she can to create a nurturing environment but has seen no improvement in her child's symptoms must feel very besieged, frustrated, and discouraged.
I believe that ADHD is a real syndrome with a strong genetic component. However, I have argued that the genetic aspect is manifested as a greater susceptibility to brain dysfunction as a consequence of insufficient fats in the diet. This includes the diet of both the child and the mother while she carried the child to term, and while she nursed the child. I believe that symptoms will improve slowly over time if the child's diet is simply adjusted to include more meats, eggs, fish, and high-fat dairy, while minimizing the consumption of empty carbs.
Unfortunately, I doubt that the symptoms will ever go away entirely, especially if the child is already a teenager by the time the change is implemented. I do not know how much of the damage in neural connections in the brain and nervous system can be repaired long after critical developmental milestones have passed. However, children's brains have been shown to be remarkably resilient after brain injury, so we can hope that significant improvement can take place over time. Of course "an ounce of prevention is worth a pound of cure." Anyone who is thinking of starting a family would be wise to change their diet in anticipation of the coming pregnancy -- to stop worrying about the mistaken belief that animal fats are unhealthy, and switch to high-fat dairy, meats, fish, and eggs instead of sugar-laden drinks and starchy foods.
I find it impossible to blame the mother for the problem -- she is only executing on both subliminal and overt messages claiming that dietary fat is unhealthy and will lead to obesity and heart disease. She is trying her best to provide her child with a healthy diet according to strong advice from both the U.S. government and the American medical establishment. I therefore expect ADHD to persist unabated in the U.S. until the authoritarian figures finally recognize and acknowledge their error, and change their tune regarding dietary fat. It is very disturbing to think of how many years it may take for them to own up to the huge mistake they have made by advocating low-fat diet, and the enormous anguish it has caused.
ADHD: References
[1] J.E. Ballard, R.A. Boileau, E.K. Sleator, B.H. Massey and R.L. Sprague, "Cardiovascular responses of hyperactive children to methylphenidate." JAMA (1976) Dec 20;236(25):2870-4.
[2] F.K. Blatchford, R.G.Knowlton, and D.A. Schneider (1985) "Plasma FFA responses to prolonged walking in untrained men and women," European Journal of Applied Physiology (1985), Vol. 53, pp. 343-347.
[3] P. R. Breggin, M.D., Talking Back to Ritalin: What Doctors aren't Telling you about Stimulants and ADHD , revised edition, Da Capo Press, Cambridge, MA, 2001.
[4] J.R. Burgess et al., "Essential fatty acid metabolism in boys with attention deficit-hyperactivity disorder," American Journal of Clinical Nutrition 1995; 62, pp. 761-68.
[5] F.X. Castellanos et al., "Developmental trajectories of brain volume abnormalities in children and adolescents with attention deficit hyperactivity disorder," JAMA (2002), Vol. 288, NO. 14, pp. 1740--1748.
[6] J. C. Chatham, "Lactate: The Forgotten Fuel," J. Physiol. (2002) Vol 542(2), p. 333.
[7] Jorge Chavarro, Walter C. Willett, and Patrick J. Skerrett, The Fertility Diet, McGraw Hill, 2008.
[8] D. Coghill and T. Banaschewski, "The genetics of attention-deficit/hyperactivity disorder," Expert Rev Neurother (2009) Oct, Vol. 9 No. 10, pp. 1547-65.
[9] B. Garcia, Y. Wei, J.A. Moron, R.Z. Lin, J.A. Javitch and A. Galli, "AKT is essential for insulin modulation of amphetamine- induced human dopamine transporter cell surface redistribution," Molecular Pharmacology (2005); DOI: 10.1124/mol.104.009092
[10] E.R. Garwood, W. Bekele, C.E. McCulloch and C.W. Christine, "Amphetamine Exposure is Elevated in Parkinson's Disease," NeuroToxicology, Vol. 27, No. 6, December 2006, Pages 1003-1006.
[11] Barry Groves, Trick and Treat: How 'Healthy Eating' is Making us Ill, Hammersmith Press, 2008.
[12] M. Guzmán and C. Blázquez, "Ketone body synthesis in the brain: possible neuroprotective effects." Prostaglandins Leukot Essent Fatty Acids (2004) Mar, Vol. 70, No. 3, pp. 287-92.
[13] E. Heininger, "A unifying hypothesis of Alzheimer's disease. IV. Causation and sequence of events," Rev Neurosci. (2000) Vol. 11 Spec No:213-328.
[14] S. Holmberg, A. Thelin and E.-L. Stiernström, "Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up," Int. J. Environ. Res. Public Health (2009) Vol. 6, pp. 2626-2638; doi:10.3390/ijerph6102626.
[15] G. Hornstra, "Essential fatty acids in mothers and their neonates," Am. J. Clin Nutr. (2000) Vol 71 (5 suppl), pp. 1262S-1269S.
[16] M. Kinsbourne, "Sugar and the hyperactive child," New England Journal of Medicine, (1994) Feb 3, pp. 355-356.
[17] A. F. La Berge, "How the Ideology of Low Fat Conquered America," Journal of the History of Medicine and Allied Sciences, (2008) Feb. 23, Vol. 63, No. 2, pp. 139-177; doi:10.1093/jhmas/jrn001
[18] N. Lambert and C.S. Hartsough, "Prospective study of tobacco smoking and substance dependence among samples of ADHD and non-ADHD subjects, Journal of Learning Disabilities (1998) Vol. 31, pp. 533-534.
[19] L. Langseth and J. Dowd, "Glucose tolerance and hyperkinesis," (1978) Food Cosmet. Toxicol. Vol. 16, p. 129.
[20] J.C. McCann and B.M.Ames BN, "Review Article: Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction," FASEB J. (2008) Vol. 22, pp. 982-1001.
[21] D. Modan-Moses, D. Stein, C. Pariente, A. Yaroslavsky, A. Ram, M. Faigin, R. Loewenthal, E. Yissachar, R. Hemi, and H. Kanety, "Modulation of Adiponectin and Leptin during Refeeding of Female Anorexia Nervosa Patients," The Journal of Clinical Endocrinology & Metabolism, Vol. 92, No. 5, pp. 1843-1847.
[22] S.H. Mostofsky, A.L. Reiss, P. Lockhart and M.B. Denckia, "Evaluation of cerbellar size in attention deficit-hyperactivity disorder," Arch. Gen. Psychiatry, (1996) Vol. 53, No. 7, pp. 607--616.
[23] V. Mougios, S. Ring, A. Petridou, and M.G. Nikolaidis, "Duration of coffee- and exercise-induced changes in the fatty acid profile of human serum," J Appl Physiol (2003) Vol. 94, pp. 476-484. doi:10.1152/japplphysiol.00624.2002
[24] H. Okuda, Y. Saito, N. Matsuoka and S. Fujii, "Mechanism of Adrenaline-induced Lipolysis in Adipose Tissue," J. Biochem, (1974) Vol. 75, No. 1, pp. 131-137.
[25] F. Ottoboni, M.P.H., Ph.D, and A. Ottoboni, Ph.D., "Can Attention Deficit-Hyperactivity Disorder Result from Nutritional Deficiency?", J. American Physicians and Surgeons, Vol. 8, No. 2, Summer, 2003.
[26] W.A. Price, Nutrition and Physical Degeneration, Los Angeles, Calif., Keats Publishing ;1998 (First Edition, 1939).
[27] B. Quistorff, N.H. Secher and J.J. Van Lieshouts, "Lactate fuels the human brain during exercise", The FASEB Journal (2008), Vol. 22, pp. 3443-3449. doi: 10.1096/fj.08-106104.
[28] U. Ravnskov, M.D., PhD, Fat and Cholesterol are Good For You,, G. B. Publishing, Sweden, 2009.
[29] A. Richardson and B. Puri, "Randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning difficulties," Prog Neuropsychopharmacol Biol Psychiatry, Vol 26(2), 2002, pp. 233-9.
[30] R.A. Robergs, and S.O. Roberts, Exercise Physiology: Exercise, Performance, & Clinical Applications, (1997) WCB McGraw-Hill, Boston, MA.
[31] P. Shaw, K. Eckstrand,W. Sharp, J. Blumenthal, J.P. Lerch, D. Greenstein, L. Clasen, A. Evans,J. Giedd and J.L. Rapoport, "Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation", Proceedings, National Academy of Sciences (2007) December 4,, Vol. 104, No. 49, pp. 19649-19654.
[32] Silver L.B. Attention-Deficit Hyperactivity disorder. Clinical guide to diagnosis and treatment. Washington: American Psychiatric Press Inc, 1992: 129-134.
[33] N. Sinn, "Physical fatty acid deficiency signs in children with ADHD symptoms," Prostaglandins Leukot Essent Fatty Acids (2007) Aug; Vol. 77 No. 2, pp. 109-15. Epub 2007 Sep 6.
[34] L.J. Stevens et al. "Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder," Am J Clin Nutr (1995) Vol. 26, No. 8, pp. 406--411.
[35] Gary Taubes, Good Calories Bad Calories:Challenging the Conventional Wisdom on Diet, Weight Control, and Disease., Alfred A. Knopf., 2007.
[36] N.D. Volkow, G.J. Wang, S.H. Kollins, T.L. Wigal, J.H. Newcorn, F. Telang, J.s. Fowler, W. Zhu, J. Logan, Y. Ma, K. Pradhan, C. Wong, and J.M. Swanson, "Evaluating dopamine reward pathway in ADHD: clinical implications." JAMA (2009) Sep 9; Vol. 302, No. 10, pp. 1084-91.
[37] N.D. Volkow, Y.-S. Ding, J.S. Fowler, G.-J. Wang, J. Logan, J.S. Gatley, S. Dewey, C. Ashby, J. Lieberman, R. Hitzemann and A.P Wolf, "Is methlphenidate like cocaine?" Archives of General Psychiatry, (1995) Vol. 52, pp. 456--463.
[38] I.T, Yamamoto and M. Sugano, "Effect of dietary fat on lipid secretion and ketone body production in rat liver," J Nutr Sci Vitaminol> (Tokyo) (1984) Apr, Vol. 30 No. 2, pp. 153-62.
[2] F.K. Blatchford, R.G.Knowlton, and D.A. Schneider (1985) "Plasma FFA responses to prolonged walking in untrained men and women," European Journal of Applied Physiology (1985), Vol. 53, pp. 343-347.
[3] P. R. Breggin, M.D., Talking Back to Ritalin: What Doctors aren't Telling you about Stimulants and ADHD , revised edition, Da Capo Press, Cambridge, MA, 2001.
[4] J.R. Burgess et al., "Essential fatty acid metabolism in boys with attention deficit-hyperactivity disorder," American Journal of Clinical Nutrition 1995; 62, pp. 761-68.
[5] F.X. Castellanos et al., "Developmental trajectories of brain volume abnormalities in children and adolescents with attention deficit hyperactivity disorder," JAMA (2002), Vol. 288, NO. 14, pp. 1740--1748.
[6] J. C. Chatham, "Lactate: The Forgotten Fuel," J. Physiol. (2002) Vol 542(2), p. 333.
[7] Jorge Chavarro, Walter C. Willett, and Patrick J. Skerrett, The Fertility Diet, McGraw Hill, 2008.
[8] D. Coghill and T. Banaschewski, "The genetics of attention-deficit/hyperactivity disorder," Expert Rev Neurother (2009) Oct, Vol. 9 No. 10, pp. 1547-65.
[9] B. Garcia, Y. Wei, J.A. Moron, R.Z. Lin, J.A. Javitch and A. Galli, "AKT is essential for insulin modulation of amphetamine- induced human dopamine transporter cell surface redistribution," Molecular Pharmacology (2005); DOI: 10.1124/mol.104.009092
[10] E.R. Garwood, W. Bekele, C.E. McCulloch and C.W. Christine, "Amphetamine Exposure is Elevated in Parkinson's Disease," NeuroToxicology, Vol. 27, No. 6, December 2006, Pages 1003-1006.
[11] Barry Groves, Trick and Treat: How 'Healthy Eating' is Making us Ill, Hammersmith Press, 2008.
[12] M. Guzmán and C. Blázquez, "Ketone body synthesis in the brain: possible neuroprotective effects." Prostaglandins Leukot Essent Fatty Acids (2004) Mar, Vol. 70, No. 3, pp. 287-92.
[13] E. Heininger, "A unifying hypothesis of Alzheimer's disease. IV. Causation and sequence of events," Rev Neurosci. (2000) Vol. 11 Spec No:213-328.
[14] S. Holmberg, A. Thelin and E.-L. Stiernström, "Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up," Int. J. Environ. Res. Public Health (2009) Vol. 6, pp. 2626-2638; doi:10.3390/ijerph6102626.
[15] G. Hornstra, "Essential fatty acids in mothers and their neonates," Am. J. Clin Nutr. (2000) Vol 71 (5 suppl), pp. 1262S-1269S.
[16] M. Kinsbourne, "Sugar and the hyperactive child," New England Journal of Medicine, (1994) Feb 3, pp. 355-356.
[17] A. F. La Berge, "How the Ideology of Low Fat Conquered America," Journal of the History of Medicine and Allied Sciences, (2008) Feb. 23, Vol. 63, No. 2, pp. 139-177; doi:10.1093/jhmas/jrn001
[18] N. Lambert and C.S. Hartsough, "Prospective study of tobacco smoking and substance dependence among samples of ADHD and non-ADHD subjects, Journal of Learning Disabilities (1998) Vol. 31, pp. 533-534.
[19] L. Langseth and J. Dowd, "Glucose tolerance and hyperkinesis," (1978) Food Cosmet. Toxicol. Vol. 16, p. 129.
[20] J.C. McCann and B.M.Ames BN, "Review Article: Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction," FASEB J. (2008) Vol. 22, pp. 982-1001.
[21] D. Modan-Moses, D. Stein, C. Pariente, A. Yaroslavsky, A. Ram, M. Faigin, R. Loewenthal, E. Yissachar, R. Hemi, and H. Kanety, "Modulation of Adiponectin and Leptin during Refeeding of Female Anorexia Nervosa Patients," The Journal of Clinical Endocrinology & Metabolism, Vol. 92, No. 5, pp. 1843-1847.
[22] S.H. Mostofsky, A.L. Reiss, P. Lockhart and M.B. Denckia, "Evaluation of cerbellar size in attention deficit-hyperactivity disorder," Arch. Gen. Psychiatry, (1996) Vol. 53, No. 7, pp. 607--616.
[23] V. Mougios, S. Ring, A. Petridou, and M.G. Nikolaidis, "Duration of coffee- and exercise-induced changes in the fatty acid profile of human serum," J Appl Physiol (2003) Vol. 94, pp. 476-484. doi:10.1152/japplphysiol.00624.2002
[24] H. Okuda, Y. Saito, N. Matsuoka and S. Fujii, "Mechanism of Adrenaline-induced Lipolysis in Adipose Tissue," J. Biochem, (1974) Vol. 75, No. 1, pp. 131-137.
[25] F. Ottoboni, M.P.H., Ph.D, and A. Ottoboni, Ph.D., "Can Attention Deficit-Hyperactivity Disorder Result from Nutritional Deficiency?", J. American Physicians and Surgeons, Vol. 8, No. 2, Summer, 2003.
[26] W.A. Price, Nutrition and Physical Degeneration, Los Angeles, Calif., Keats Publishing ;1998 (First Edition, 1939).
[27] B. Quistorff, N.H. Secher and J.J. Van Lieshouts, "Lactate fuels the human brain during exercise", The FASEB Journal (2008), Vol. 22, pp. 3443-3449. doi: 10.1096/fj.08-106104.
[28] U. Ravnskov, M.D., PhD, Fat and Cholesterol are Good For You,, G. B. Publishing, Sweden, 2009.
[29] A. Richardson and B. Puri, "Randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning difficulties," Prog Neuropsychopharmacol Biol Psychiatry, Vol 26(2), 2002, pp. 233-9.
[30] R.A. Robergs, and S.O. Roberts, Exercise Physiology: Exercise, Performance, & Clinical Applications, (1997) WCB McGraw-Hill, Boston, MA.
[31] P. Shaw, K. Eckstrand,W. Sharp, J. Blumenthal, J.P. Lerch, D. Greenstein, L. Clasen, A. Evans,J. Giedd and J.L. Rapoport, "Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation", Proceedings, National Academy of Sciences (2007) December 4,, Vol. 104, No. 49, pp. 19649-19654.
[32] Silver L.B. Attention-Deficit Hyperactivity disorder. Clinical guide to diagnosis and treatment. Washington: American Psychiatric Press Inc, 1992: 129-134.
[33] N. Sinn, "Physical fatty acid deficiency signs in children with ADHD symptoms," Prostaglandins Leukot Essent Fatty Acids (2007) Aug; Vol. 77 No. 2, pp. 109-15. Epub 2007 Sep 6.
[34] L.J. Stevens et al. "Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder," Am J Clin Nutr (1995) Vol. 26, No. 8, pp. 406--411.
[35] Gary Taubes, Good Calories Bad Calories:Challenging the Conventional Wisdom on Diet, Weight Control, and Disease., Alfred A. Knopf., 2007.
[36] N.D. Volkow, G.J. Wang, S.H. Kollins, T.L. Wigal, J.H. Newcorn, F. Telang, J.s. Fowler, W. Zhu, J. Logan, Y. Ma, K. Pradhan, C. Wong, and J.M. Swanson, "Evaluating dopamine reward pathway in ADHD: clinical implications." JAMA (2009) Sep 9; Vol. 302, No. 10, pp. 1084-91.
[37] N.D. Volkow, Y.-S. Ding, J.S. Fowler, G.-J. Wang, J. Logan, J.S. Gatley, S. Dewey, C. Ashby, J. Lieberman, R. Hitzemann and A.P Wolf, "Is methlphenidate like cocaine?" Archives of General Psychiatry, (1995) Vol. 52, pp. 456--463.
[38] I.T, Yamamoto and M. Sugano, "Effect of dietary fat on lipid secretion and ketone body production in rat liver," J Nutr Sci Vitaminol> (Tokyo) (1984) Apr, Vol. 30 No. 2, pp. 153-62.
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