The fallacy of using DHA alone for brain trauma

I am constantly amazed by the lack of understanding by neurologists of basic essential fatty acid biochemistry in the treatment of brain trauma and concussions. They often blindly believe that the only omega-3 fatty acid that has any impact in the treatment of concussions is DHA alone. Their blind faith is based on the observation that you find a lot of DHA in the brain and little EPA. This obviously means that EPA must not be important for brain function. This is similar to stating the world is flat because it appears that way to the naked eye.

I have mentioned many times in my books that EPA and DHA have different functions, and that’s why you need both of these essential omega-3 fatty acids (1-4). This is especially true for the brain. EPA produces most of the anti-inflammatory properties of omega-3 fatty acids since it’s structurally similar to arachidonic acid (AA) as they both contain 20 carbon atoms with approximately the same spatial configuration. As a result, EPA can inhibit the enzymes that would otherwise produce pro-inflammatory eicosanoids from AA. It is AA that generates the inflammation caused by brain trauma. DHA, on the other hand, is primarily a structural component of neural tissue. They do different jobs, and that’s why you need both in combination.

So why isn’t there as much EPA in the brain compared to DHA? The reason is simple. EPA enters the brain just as quickly as DHA, but it is rapidly oxidized, whereas DHA is sent off to long-term storage in neural tissue (5-7). The lifetime of DHA in the human brain is measured in years, whereas the lifetime of the EPA is measured in days. So obviously when you kill an animal and look at the brain, you are not going to find very much EPA.

What complicates the issue is that if you only treat a concussion with DHA, some of the DHA will be converted to EPA. This gives the appearance that DHA is working to reduce inflammation. Since brain trauma and concussions generate inflammation in the brain, doesn’t it make more sense to provide as much EPA as possible to reduce the inflammation as opposed to supplementing only with DHA and hoping some fraction of it will be converted to EPA?

To answer that question, it is useful to look at two recent studies that used the same protocol to study inflammation induced by a concussion injury (8,9). The same total amount of omega-3 fatty acids was used to treat the animals after the concussion injury. One experiment used a 2:1 ratio of EPA to DHA, and the other experiment used only DHA. If the DHA was so important, then the animals treated with the DHA alone should have demonstrated three times the reduction of neuro-inflammation compared to the group that received omega-3 fatty acids containing only one-third as much DHA.

In fact, just the opposite was the case. The 2:1 EPA/DHA group demonstrated greater benefits compared to the DHA-alone group in reducing neuro-inflammation induced by a concussion. Why? EPA is a far more powerful anti-inflammatory agent than DHA. This is why in both studies the AA/EPA ratio was used as the marker of inflammation induced by the concussion injury. Since the AA/EPA ratio was decreased in both studies, this meant that some of the pure DHA was converted to EPA providing at least some anti-inflammatory actions. Thus giving 100 percent DHA is not exactly the most efficient way to decrease neuro-inflammation induced by a concussion injury. This is further emphasized by a recent study that indicated that 1 gram of DHA per day for an 18-month period had no impact in the cognitive improvement of Alzheimer’s patients (10), even though Alzheimer’s is known to be a neuro-inflammatory disease (11).

Does this mean that DHA is not important for brain repair? Of course not. This is because you need both EPA and DHA for optimal repair of brain damage after a concussion. You need the EPA to reduce the neuro-inflammation, and you need the DHA to help rebuild new neurons. But to give DHA alone without additional EPA to maximally reduce neuro-inflammation caused by concussions simply makes no sense.

References

  1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  2. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  3. Sears B. “The Anti-inflammation Zone.” Regan Books. New York, NY (2005)
  4. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  5. Chen CT, Liu Z, and Bazinet RP. “Rapid de-esterification and loss of eicosapentaenoic acid from rat brain phospholipids: an intracerebroventricular study.” J Neurochem 116: 363-373 (2011)
  6. Chen CT, Liu Z, Ouellet M, Calon F, and Bazinet RP. “Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study. “Prostaglandins Leukot Essent Fatty Acids 80: 157-163 (2009)
  7. Umhau JC, Zhou W, Carson RE, Rapoport SI, Polozova A, Demar J, Hussein N, Bhattacharjee AK, Ma K, Esposito G, Majchrzak S, Herscovitch P, Eckelman WC, Kurdziel KA, and Salem N. “Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography.” J Lipid Res 50: 1259-1268 (2009)
  8. Mills JD, Bailes JE, Sedney CL, Hutchins H, and Sears B. “Omega-3 fatty acid supplementation and reduction of traumatic axonal injury in a rodent head injury model.” J Neurosurg 114: 77-84 (2011)
  9. Bailes JE and Mills JD. “Docosahexaenoic acid reduces traumatic axonal injury in a rodent head injury model.” J Neurotrauma 27: 1617-1624 (2010)
  10. Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, and Aisen PS. “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.” JAMA 304: 1903-1911 (2010)
  11. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, Cooper NR, Eikelenboom P, Emmerling M, Fiebich BL, Finch CE, Frautschy S, Griffin WS, Hampel H, Hull M, Landreth G, Lue L, Mrak R, Mackenzie IR,McGeer PL, O’Banion MK, Pachter J, Pasinetti G, Plata-Salaman C, Rogers J, Rydel R, Shen Y, Streit W, Strohmeyer R, Tooyoma I, Van Muiswinkel FL,Veerhuis R, Walker D, Webster S, Wegrzyniak B, Wenk G, and Wyss-Coray T. “Inflammation and Alzheimer’s disease.” Neurobiol Aging 21: 383-421 (2000)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Obesity starts in the womb

A new study from Harvard Medical School strongly suggests that childhood obesity begins in the mother’s womb (1). Specifically, the lower the EPA and DHA concentrations in either the mother’s diet or her umbilical cord attached to the fetus, the more likely the child will develop obesity by age 3.

It is well known from animal experiments that omega-6 fatty acids make the offspring fat, and omega-3 fatty acids make the offspring thin (2-4). This new study now confirms the same thing is happening in humans (1).

It has been demonstrated in animal models that it only takes three to four generations of a high omega-6 fatty acid intake to increase obesity in the offspring (5,6). I believe one of the driving forces for the increase in childhood obesity has been the dramatic increase in omega-6 fatty acids over the past 100 years (7). However, much of that omega-6 fatty acid increase has come from the massive increase in soybean oil consumption that started in the early 1970s. That 40-year period only represents about two generations of humans, which means it is quite likely there will be higher childhood obesity rates coming with the next generations as long as omega-6 fatty acid consumption stays elevated.

At the molecular level, the problem really starts when these excess omega-6 fatty acids are activated by ever-increasing insulin levels caused by refined carbohydrate consumption to create increased cellular inflammation. In my book “Toxic Fat“ I describe some of the political decisions and their metabolic consequences that have led to the epidemic increase of cellular inflammation that has resulted in the rapid deterioration of American health (8).

The bottom line is that this dramatic increase in omega-6 fatty acids in the diet of American mothers is causing trans-generation changes in our children due to fetal programming. This occurs in the womb and results in the final tuning of the genetic code of the fetus by changing the gene expression of the unborn child. This is called epigenetic programming and begins to explain why each succeeding generation of Americans is getting fatter and fatter (9).

Even more ominous warnings are animal studies that indicate the “reward” response (increased dopamine levels) induced by consuming junk food experienced by the mother can also be transferred to the next generation by fetal programming (10).

So what can you do about this growing genetic disaster? If you are contemplating having a child, then beginning to cut back on omega-6 fatty acids and eating more omega-3 fatty acids is a good starting point. The benefits include having a thinner and smarter child. If you already have children whose gene expression has already been altered by fetal programming, then you have to control their diet for a lifetime to prevent reverting to that altered gene expression. It’s not a pretty picture. Although you can’t escape the dietary consequences of fetal programming, you can minimize the damage by treating food as drug to manage increased cellular inflammation that is making us fatter, sicker and dumber.

References

  1. Donahue, SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gillman MW, and Oken E. “Prenatal fatty acid status and child adiposity at age 3y.” Amer J Clin Nutr 93: 780-788 (2011)
  2. Gaillard D, Negrel R, Lagarde M and Ailhaud G. “Requirement and role of arachidonic acid in the differentiation of pre-adipose cells.” Biochem J 257: 389-397 (1989)
  3. Kim HK, Della-Fera M, Lin J, and Baile CA. “Docosahexaenoic acid inhibits adipocyte differentiation and induces apoptosis in 3T3-L1 pre-adipocytes.” J Nutr 136: 2965-2969 (2006)
  4. Massiera F, Saint-Marc P, Seydoux J, Murata T, Kobayashi T, Narumiya S, Guesnet P, Amri EZ, Negrel R, and Ailhaud G. “Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?” J Lipid Res 44: 271-279 (2003)
  5. Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, and Rawlings RR. “Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century.” Am J Clin Nutr 93: 950-962 (2011)
  6. Hanbauer I, Rivero-Covelo I, Maloku E, Baca A, Hu Q, Hibbeln JR, and Davis JM. “The Decrease of n-3 Fatty Acid Energy Percentage in an Equicaloric Diet Fed to B6C3Fe Mice for Three Generations Elicits Obesity.” Cardiovasc Psychiatry Neurol: 2009, Article ID.867041 (2009)
  7. Massiera F, Barbry P, Guesnet P, Joly A, Luquet S, Moreilhon-Brest C, Mohsen-Kanson T, Amri EZ, and Ailhaud G. “A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations.” J Lipid Res 51: 2352-2361 (2010)
  8. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  9. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C, Rodford J, Slater-Jefferies J, Garratt E, Crozier SR, Emerald BS, Gale CR, Inskip HM, Cooper C, and Hanson MA. “Epigenetic gene promoter methylation at birth is associated with child’s later adiposity.” Diabetes 60: 1528-1534 (2011)
  10. Ong ZY and Muhlhausler BS. “Maternal “junk-food” feeding of rat dams alters food choices and development of the mesolimbic reward pathway in the offspring.” FASEB J 25: S1530-6860 (2011)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Fetal programming: Gene transformation gone wild (Part II)

In part 1 of this blog, I discussed how dietary changes can alter gene expression and how those epigenetic changes can be mediated from one generation to the next by fetal programming. This is very clear from animal studies. One of the most frightening studies was published a few years ago (1). In this study, genetically identical mice were split into two colonies. For the next three generations they were fed exactly the same number of calories with exactly the same balance of protein, carbohydrate, and fat. The only difference was that one group had a diet rich in omega-6 fatty acids and low in omega-3 fatty acids, and the other had a better balance of omega-3 to omega-6 fatty acids. After three generations the mice fed the high omega-6 fatty acid diet were grossly obese.

In addition, the mice with high omega-6 fatty acids had fatty livers and enlarged hearts and kidneys, all indicative of major metabolic disturbances.

This also happens with the brain. It has been demonstrated that removing omega-3 fatty acids and replacing them with omega-6 fatty acids over three generations makes animals a lot dumber, probably due to significant reductions in neurotransmitters, like serotonin and dopamine (2-5). Not only are they dumber, but their offspring also show a strong preference for junk food. (6)

How could this happen in such a short period of time? The answer is fetal programming induced by increased cellular inflammation. If this cellular inflammation is maintained by an inflammatory diet, there will be a constant driving force to maintain these epigenetic effects from one generation to other.

The next question is how long does this epigenetic programming have to be continued until it becomes a permanent part of the gene structure. One indication might be found in the development of lactose intolerance in those populations who have been exposed to dairy products for thousands of years. Seventy percent of the world’s population can’t digest these dietary products because they have lost the ability to maintain the necessary enzyme production after weaning from mother’s breast milk. Those who have been constantly exposed to dairy products after weaning have developed an epigenetic programming that seems to be permanent.

These epigenetic changes in humans may take place in only one generation. This is the suggestion of a new article to be published in Diabetes that indicates more than 25 percent of the explanation for childhood obesity could be predicted by prenatal epigenetic changes at birth (7).

As long as our epidemic of cellular inflammation continues to be fueled by the Perfect Nutrition Storm, we can expect our children to continue to become fatter, sicker, and dumber (8).

References

  1. Hanbauer I, Rivero-Covelo I, Maloku E, Baca A, Hu Q, Hibbeln JR, and Davis JM. “The Decrease of n-3 Fatty Acid Energy Percentage in an Equicaloric Diet Fed to B6C3Fe Mice for Three Generations Elicits Obesity.” Cardiovasc Psychiatry Neurol: 2009, Article ID.867041 (2009)
  2. Chalon S, Delion-Vancassel S, Belzung C,,Guilloteau D, Leguisquet AM, Besnard JC, and Durand G. “Dietary fish oil affects monoaminergic neurotransmission and behavior in rats.” J Nutr 128: 2512-2519 (1998)
  3. Zimmer L, Delpal S, Guilloteau D, Aioun J, Durand G, and Chalon S. “Chronic n-3 polyunsaturated fatty acid deficiency alters dopamine vesicle density in the rat frontal cortex.” Neurosci Lett 284: 25-28 (2000)
  4. Moriguchi T, Greiner RS, and Salem N. “Behavioral deficits associated with dietary induction of decreased brain docosahexaenoic acid concentration.” J Neurochem 75: 2563-2573 (2000)
  5. Chalon S. “Omega-3 fatty acids and monoamine neurotransmission.” Prostaglandins Leukot Essent Fatty Acids 75: 259-269 (2006)
  6. Ong ZY and Muhlhausler BS. “Maternal “junk-food” feeding of rat dams alters food choices and development of the mesolimbic reward pathway in the offspring.” FASEB J 25: S1530-6860 (2011)
  7. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C, Rodford J, Slater-Jefferies J, Garratt E, Crozier SR, Emerald BS, Gale CR, Inskip HM, Cooper C, and Hanson MA. “Epigenetic gene promoter methylation at birth is associated with child’s later adiposity.” Diabetes 60: doi: 10.2337/db10-0979 (2011)
  8. Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD, and Hanson MA. “Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease.” Pediatr Res 61: 5R-10R (2007)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Fish oil and fat loss

I have often said, “It takes fat to burn fat”. As I describe in my book “Toxic Fat,” increased cellular inflammation in the fat cells turns them into “fat traps” (1). This means that fat cells become increasingly compromised in their ability to release stored fat for conversion into chemical energy needed to allow you to move around and survive. As a result, you get fatter, and you are constantly tired and hungry.

One of the best ways to reduce cellular inflammation in the fat cells is by increasing your intake of omega-3 fatty acids. This was demonstrated in a recent article that indicated supplementing a calorie-restricted diet with 1.5 grams of EPA and DHA per day resulted in more than two pounds of additional weight loss compared to the control group in a eight-week period (2).

How omega-3 fatty acids help to ”burn fat faster” is most likely related to their ability to reduce cellular inflammation in the fat cells (3,4) and to increase the levels of adiponectin (5). Both mechanisms will help relax a “fat trap” that has been activated by cellular inflammation.

However, there is a cautionary note. This is because omega-3 fatty acids are very prone to oxidation once they enter the body. This is especially true relative to the enhanced oxidation of the LDL particles (6-9).

This means that to get the full benefits any fish oil supplementation, you have to increase your intake of polyphenols to protect the omega-3 fatty acids from oxidation. How much? I recommend at least 8,000 additional ORAC units for every 2.5 grams of EPA and DHA that you add to your diet. That's about 10 servings per day of fruits and vegetables, which should be no problem if you are following the Zone diet. If not, then consider taking a good polyphenol supplement.

Once you add both extra fish oil and polyphenols to a calorie-restricted diet, you will burn fat faster without any concern about increased oxidation in the body that can lead to accelerated aging.

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, and Martinez JA. “Randomized trial of weight-loss diets for young adults varying in fish and fish oil content.” Int J Obes 31: 1560-1566 (2007)
  3. Huber J, Loffler M, Bilban M, Reimers M, Kadl A, Todoric J, Zeyda M, Geyeregger R, Schreiner M, Weichhart T, Leitinger N, Waldhausl W, and Stulnig TM. “Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids.” Int J Obes 31: 1004-1013 (2007)
  4. Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhausl W, and Stulnig TM. “Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids.” Diabetologia 49: 2109-2119 (2006)
  5. Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, and Jebb SA. “Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women.” Int J Obes 30: 1535-1544 (2006)
  6. Pedersen H, Petersen M, Major-Pedersen A, Jensen T, Nielsen NS, Lauridsen ST, and Marckmann P. “Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes.” Eur J Clin Nutr 57: 713-720 (2003)
  7. Turini ME, Crozier GL, Donnet-Hughes A, and Richelle MA. “Short-term fish oil supplementation improved innate immunity, but increased ex vivo oxidation of LDL in man–a pilot study.” Eur J Nutr 40: 56-65 (2001)
  8. Stalenhoef AF, de Graaf J, Wittekoek ME, Bredie SJ, Demacker PN, and Kastelein JJ. “The effect of concentrated n-3 fatty acids versus gemfibrozil on plasma lipoproteins, low-density lipoprotein heterogeneity and oxidizability in patients with hypertriglyceridemia.” Atherosclerosis 153: 129-138 (2000)
  9. Finnegan YE. Minihane AM, Leigh-Firbank EC, Kew S, Meijer GW, Muggli R, Calder PC, and Williams CM. “Plant- and marine-derived n-3 polyunsaturated fatty acids have differential effects on fasting and postprandial blood lipid concentrations and on the susceptibility of LDL to oxidative modification in moderately hyperlipidemic subjects.” Am J Clin Nutr 77: 783-795 (2003)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Fetal programming: Gene transformation gone wild (Part I)

Normally genes change very slowly through mutation. Most mutations are harmful and hence provide no survival advantage to the organism. This is why there is a less than a 2 percent difference between our genes and those of a chimpanzee, even though we became a separate species more than six million years ago. What distinguishes mankind is not the number of genes (corn has twice as many genes as humans), but the speed at which our genes can be turned on and off. This is because of the presence of gene transcription factors that can be activated or inhibited by nutrients. The effect of nutrients on gene expression is known as nutrigenomics.

Because of mankind’s rapid gene switching abilities, gene expression can be influenced significantly by the diet. Due to the speed at which new food ingredients are being introduced into the human diet, these types of nutrigenomic interactions can create radical changes in gene expression in a very short period of time. Normally what a person eats should only affect their gene expression during their lifetime. But is it possible that these changes in genetic expression can be transferred to the next generation?

We can see how genetic engineering (i.e. cross-breeding) can rapidly change the size and shape of dogs, flowers, vegetables and fruits. The genes in each of these species don’t change, but changes in gene expression induced by crossbreeding can persist from one generation to the next, especially if they are constantly reinforced. This is known as epigenetics.

Somehow we don’t think this type of epigenetic change can happen to us, but it does as a result of fetal programming. The prenatal period in the womb is the time that a child’s genes are most susceptible to epigenetic programming. Epigenetic programming can be amplified by the ongoing dietary effects on gene transcription factors (i.e. nutrigenomics) taking place in the mother. The result is the imprinting of epigenetic changes on the genes of the developing fetus that can alter the metabolic future of the child (1).

Examples of how this type of epigenetic programming influences future metabolic effects has been demonstrated under the conditions of famine, which generate increased obesity and cardiovascular disease in the next generation (2). This is also true of children who were exposed to excess calories or elevated levels of glucose while they were developing in the womb (3,4). Likewise hypertension (i.e. pre-eclampsia) during pregnancy increases the risk of stroke as adults if the fetus is exposed to the high blood pressure in the womb (5) as well as the increased risk of adult obesity if the fetus is exposed to gestational diabetes in the mother (6).

Bottom line: The dietary and metabolic environment the fetus is exposed to in the womb can echo through the rest of his or her life. In part II of this blog, I will explore how the Perfect Nutritional Storm, described in my book “Toxic Fat” (7) has been making Americans fatter, sicker and dumber for the last three generations.

References

  1. Kussman M, Krause L, and Siffert W. “Nutrigenomics: where are we with genetic and epigenic markers for disposition and susceptibility?” Nutrition Rev 68: S38-S47 (2010)
  2. Painter RC, Roseboom TJ, and Bleker OP. “Prenatal exposure to the Dutch famine and disease in later life.” Reprod Toxicol 20: 345-352 (2005)
  3. Singhal A. “Early nutrition and long-term cardiovascular health.” Nutrition Rev 64: S44-S49 (2006)
  4. Boney CM, Verma A, Tucker R, and Bovh BR. “Metabolic syndrome in childhood: associated with birth weight, maternal obesity, and gestational diabetes mellitus.” Pediatrics 115: e290-e296 (2005)
  5. Kajantie E, Eriksson JG, Osmond C, Thornburg K, and Barker DJP. “Pre-eclampsia is associated with increased risk of stroke in the adult offspring.” Stroke 40: 1176-1180 (2009)
  6. Lawlor DA, Pichtenstein P, and Langstrom N. “Association of maternal diabetes mellitus in pregnancy with offspring adiposity into early adulthood.” Circulation 123: 258-265 (2011)
  7. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

A new obesity suspect

The number of overweight and obese has been remarkably stable for the past several years at about two-thirds of the adult population. This strongly suggests that these Americans are genetically prone to gain weight under the right dietary circumstances. Yet a greater number of adults are moving from a classification of being simply overweight to being labeled as obese. This is a strong indication that those who are genetically predisposed to weight gain are becoming fatter. According to the Centers for Disease Control, only three states in 2007 had more than 30 percent of the adult population classified as obese. In only two years, the number of states that have more than 30 percent obesity in adult populations had increased to nine. That’s a 300 percent increase in two years!

One new suspect in our growing obesity crisis may be caffeinated coffee. It has been known for a long time that a high-fat meal increases blood sugar as well as maintains high levels of triglycerides (1). A new study from the University of Guelph found that consuming a high-fat meal increased blood sugar by more than 30 percent when giving a standard glucose tolerance test five hours later (2). Adding the equivalent of two cups of coffee more than doubled this increase in blood-sugar levels five hours after a high-fat meal.

The implication is that a constant diet of high-fat foods and a lot of coffee will accelerate the development of insulin resistance. When this occurs, the pancreas is forced to release more insulin to help reduce blood sugar levels. Unfortunately, it is excess insulin that makes you fat and keeps you fat.

The controversy over caffeine has continued for more than 100 years. The first instance occurred in a trial in the early part of the 20th century at which the U.S. government sued Coca-Cola for adulterating a food by adding caffeine to a soft drink. (Fortunately for Coca-Cola, the company had removed the coca extracts containing cocaine several years earlier). In a trial similar to the Scopes trial on evolution that would be held 15 years later in the same court system, the testimony was highly charged on both sides. The local judge dismissed the case, but the government continued it for many years in various appeals courts until the case was settled with a no-contest plea (3).

Now a new call for limits on caffeine was presented in a recent article in the Journal of the American Medical Association (4). Maybe with more research we will find that caffeine may be another factor for those who are genetically predisposed to gain weight to become fatter than ever.

References:

  1. Tushuizen ME, Nieuwland R, Scheffer PG, Sturk A, Heine RJ, and Diamant M. “Two consecutive high-fat meals affect endothelial-dependent vasodilation, oxidative stress and cellular microparticles in healthy men.” J Thromb Haemost 4: 1003-1010 (2006)
  2. Beaudoin MS, Robinson LE, and Graham TE. “An oral lipid challenge and acute intake of caffeinated coffee additively decrease glucose tolerance in healthy men.” J Nutrition 141: 574-581 (2011)
  3. Carpenter M. “A century later, jury’s still out on caffeine limits.” New York Times. March 28, 2011
  4. Arria A and O’Brien MC. “The ‘high’ risk of energy drinks.” JAMA 305: 600-601 (2011)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Omega-3 fatty acids and blood pressure

Blood Pressure CuffIt was recognized many years ago that fish oil has a dose-dependent effect on lowering blood pressure (1). So how does it do it? There are a lot of different ways.

The first is the ability of the omega-3 fatty acids in fish oil to alter the levels of a group of hormones known as eicosanoids (2,3). These are the hormones that cause blood vessels to contract, thereby increasing the pressure needed to pump blood through the arteries. The omega-3 fatty acids, especially eicosapentaenoic acid (EPA), inhibit both the synthesis and release of the omega-6 fatty acid arachidonic acid (AA) that is the molecular building block necessary to produce those eicosanoids that cause constriction of blood vessels.

The second way that fish oil helps reduce blood pressure is to accelerate weight loss. When you lose excess weight, blood pressure invariably decreases. A recent trial has indicated that when you add fish oil to a calorie-restricted diet, there is greater weight loss (4). This study was followed by an additional trial that indicated when adding fish oil to a weight-reduction diet, there was a further effect on lowering blood pressure (5). So how does fish oil help you lose excess weight? The answer lies in the ability of the omega-3 fatty acids in fish oil to reduce cellular inflammation in the fat cells (6). It's that cellular inflammation that makes you fat and keeps you fat. Reducing that cellular inflammation in the fat cells is the key to weight loss.

Finally another cause of increased blood pressure is increased stress. It was shown in 2003 that high levels of fish oil reduce the rise of blood pressure induced by mental stress (7).

Of course, the best way to reduce blood pressure is to follow an anti-inflammatory diet rich in omega-3 fatty acids. That means a diet rich in fruits and vegetables with adequate levels of low-fat protein and low levels of omega-6 and saturated fats. It's also commonly known as the Zone diet.

References:

  1. Morris MC, Sacks F, and Rosner B. “Does fish oil lower blood pressure? A meta-analysis of controlled trials.” Circulation 88: 523-533 (1993)
  2. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  3. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  4. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, and Martinez JA. “Randomized trial of weight-loss diets for young adults varying in fish and fish oil content.” Int J Obes 31: 1560-1566 (2007)
  5. Ramel A, Martinez JA, Kiely M, Bandarra NM, and Thorsdottir I. “Moderate consumption of fatty fish reduces diastolic blood pressure in overweight and obese European young adults during energy restriction.” Nutrition 26: 168-174 (2010)
  6. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  7. Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, and Tappy L. “Fish oil prevents the adrenal activation elicited by mental stress in healthy men.” Diabetes Metab 29: 289-295 (2003)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

New solution or simply admitting failure?

SurgeryLast week the International Diabetes Federation (IDF) announced that gastric bypass surgery is a cost-effective treatment for type 2 diabetes. This marks the first time in modern medicine that cutting out normal tissue is now considered good medicine. It also indicates the pathetic state of medical science for the treatment of diabetes.

Make no mistake: Type 2 diabetes is now a pandemic, affecting approximately 300 million people worldwide. This is projected to increase to some 450 million people worldwide by 2030. Since diabetes is one of the most costly chronic disease conditions, it is the most likely to break the financial backbone of health-care systems in every advanced country.

The typical gastric bypass surgery costs from $15,000 to $24,000. Just for argument's sake, let's assume it is $20,000 for each surgery. Since some 26 million people in the United States have type 2 diabetes, then a mere $520 billion dollars spent on gastric bypass surgery would solve our growing epidemic. Obviously we don't have that type of money floating in the health-care system.

Furthermore, the 10-year failure rate is relatively high for this type of surgery (1). For example, 20 percent of patients who were initially obese (BMI >50 percent) could not maintain their long-term BMI below 35 percent (the definition of morbidly obese). This failure rate rises to 58 percent for those whose initial BMI was greater than 50.

The key feature as to why gastric bypass surgery works is the almost immediate suppression of hunger, mediated by improved release of hormones from the gut (i.e. PYY) that go directly to the brain to tell the patient to stop eating. Over time it would appear that this initial enhancement of PYY release is being compromised. As a result, those patients regain the lost weight.

So maybe gastric bypass is not the best long-term solution (and definitely not a cost-effective one in those patients that regain much of their lost weight) for solving the current epidemic of diabetes. So what's the alternative? One solution would be an anti-inflammatory diet that supplies adequate protein to stimulate PYY release as well as control the levels of cellular inflammation in the pancreas, the underlying reason why insufficient insulin levels are secreted in the first place (2).

Call me crazy, but this dietary approach appears far more cost-effective.

References

  1. Christou NV, Look D, and MacLean LD. “Weight gain after short- and long-limb gastric bypass in patients followed for longer than 10 years.” Ann Surg 244: 734-740 (2006)
  2. Donath MY,Boni-Schnetzler M, Ellingsgaard H, and Ehses JA. “Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.” Physiology 24: 325-331 (2009)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Mythologies in treatment of childhood obesity

childhood obesityWe all know that obese children tend to be inactive. This leads to the “obvious” conclusion that the solution to childhood obesity is simply more exercise. But what if that conclusion is totally wrong?

There is no mistaking that obesity and lack of physical activity are linked. But which comes first? The answer appears to be obesity (1). A study published online in the Archives of Disease in Childhood followed young children over a four-year period carefully measuring their physical activity with accelerometers to measure physical activity for seven consecutive days as well as their percentage of body fat using DEXA scans. What they found was that physical inactivity was not related to the increased accumulation of body fat, rather they found that increased body fat was the cause of decreasing physical activity. This is also the situation with adults (2-5).

So why do so many researchers believe that inactivity leads to fatness? Because it just has to be the answer. This belief persists in spite of numerous studies that demonstrate that increased physical activity has little impact on reducing childhood obesity (6). This is a classic case of don't confuse me with the facts, since in my heart I know I am right.

This is not to say that exercise has no benefits in obese children. In fact, the same authors had published an earlier study indicating that while intense exercise had little impact on fat loss, there is a significant benefit in reducing insulin resistance (7).

The implications of this study in children are immense. In essence, increasing public expenditures to increase physical activity will not address the childhood obesity epidemic no matter how much money you throw at the problem. Instead you have to focus on reducing calorie intake. However, this decrease in calorie consumption is not going to be accomplished by increased willpower, but by increasing satiety (lack of hunger) in obese children.

As I pointed out in my most recent book, “Toxic Fat,” if you want to increase satiety, you must reduce cellular inflammation in the brain (8). That is best accomplished by a combination of an anti-inflammatory diet coupled with high-dose fish oil.

Of course, as an alternative, you could always consider gastric bypass surgery.

References

  1. Metcalf BS, Hosking J, Jeffery AN, Voss LD, Henley W, and Wilkin TJ. “Fatness leads to inactivity, but inactivity does not lead to fatness.” Arch Dis Chil doi:10.1136/adc.2009.175927
  2. Bak H, Petersen L, and Sorensen TI. “Physical activity in relation to development and maintenance of obesity in men with and without juvenile onset obesity.” Int J Obes Relate Metabl Disord 28: 99-104 (2004)
  3. Petersen L, Schnorhr, and Sorensen TI. “Longitudinal study of the long-term relation between physical activity and obesity in adults.” Int J Obes Relate Metabl Disord 28: 105-112 (2004)
  4. Mortensen LH, Siegler Ic, Barefoot JC, Gronbaek M, and Sorensen TI. “Prospective associations between sedentary lifestyle and BMI in midlife.” Obesity 14: 1462-1471 (2006)
  5. Ekelund U, Brage S, Besson H, Sharp S, and Wareham NJ. “Time spent being sedentary and weight gain in healthy adults.” Am J Clin Nutr 88: 612-617 (2008)
  6. Wareham NJ, van Sluijs EM, and Ekelund U. “Physical activity and obesity prevention: a review of the current evidence.” Proc Nutr Soc 64: 229-247 (2005)
  7. Metcalf BS, Voss LD, Hosking J, Jeffery AN, and Wilkin TJ. “Physical activity at the government-recommended level and obesity-related outcomes.” Arch Dis Child93: 772-777 (2008)
  8. Sears B. “Toxic Fat”. Thomas Nelson. Nashville, TN (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

A really dumb diet from France

After experiencing so many years of ridicule (now effectively past history) with the Zone diet, I never thought I would possibly criticize another new diet unless it was either dangerous or just plain foolish. The newest diet from France is both.

Called the Dukan diet, this program is a strange combination of the Atkins diet with a French twist. As usual, there are number of diet phases that have to be followed. The first one is downright dangerous as it recommends unlimited amounts of lean protein, 1½ tablespoons of oat bran and lots of water. The reason this phase is dangerous is because there are virtually no carbohydrates or fats to counterbalance the protein. My best estimate is in this first phase more than 90 percent of the total calories are coming from protein. This will overwhelm the liver's capacity to metabolize the excess protein leading to a condition known as “rabbit starvation” (1). This was a condition experienced by early Arctic explorers who only subsisted on lean protein. They quickly became dehydrated as the body desperately tried to excrete excess ammonia (the first breakdown product of protein) through the urine that could not be converted to urea by the liver. This leads to dehydration, diarrhea, nausea, low blood pressure and fatigue. At least on the Atkins diet there was a lot of fat coupled with the protein to help the liver metabolize the ammonia from the protein into urea that could be easily removed in the urine.

The dehydration from such a severely ketogenic diet explains the need for lots of water. As far as the oat bran, it contains virtually no carbohydrate, but lots of soluble fiber to help expand the stomach. Yes you will lose weight (primarily water) and insulin levels in the blood will drop dramatically, but you will reduce the elasticity of the blood vessels (2) and increase insulin resistance in the liver (3). The decrease in the elasticity of blood vessels increases the likelihood of a heart attack, (4) and the growing insulin resistance sets the stage for liver dysfunction that always promotes weight regain. This first phase is called the Attack Phase, I assume because it attacks your liver and your metabolism.

Phase 2 of this diet is just as wacky. Now you increase the oat bran to 2 tablespoons per day and have some vegetables every other day. This phase remains a highly ketogenic diet, meaning the liver and blood vessels are still in a metabolic mess. This is called the Cruise Phase. I guess this means you are cruising for a hard landing even though you are still losing weight.

If you last through the first two phases (about two months), you enter into the Consolidation Phase that is just as wacky as the Cruise Phase, but in the other direction. Now you can add non-starchy vegetables every day and a piece of fruit (I applaud these additions). But then why does this diet let the person start eating bread every day and rice and pasta twice a week plus two Porky Pig meals including dessert and wine (that's the French twist). It's like an insidious plot to demonstrate how quickly you will regain the lost weight, but now as newly synthesized fat. Of course, by following this Consolidation Phase, it is virtually guaranteed you will consolidate the lost weight into new stored fat.

Finally, there is the Stabilization Phase where you can eat anything you want (mac and cheese, fried chicken, etc.) as long as you eat only lean protein one day each week. Fat chance you will ever get there.

You probably won't die on the Dukan diet, but you will mess up your liver metabolism making it much more difficult to lose the resulting regain of fat mass on the Consolidation Phase.

I am frankly getting a cold sweat as I write this blog since I am sounding a lot like Dean Ornish yelling at Bob Atkins in the old days. But even Bob would say the Dukan diet is just plain stupid.

References

  1. Silsborough S and Mann N. “A review of issues of dietary protein intake in humans.” Int J Sports Nutr Exerc Metab 16: 129-152 (2006)
  2. Buscemi S, Verga S, Tranchina MR, Cottone S, and Cerasola G. “Effects of hypocaloric very-low-carbohydrate diet vs. Mediterranean diet on endothelial function in obese women.” Eur J Clin Invest 39: 339-347 (2009)
  3. Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D; Zhang XM, Samuel VT, and Shulman GI. “A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.” Am J Physiol Endocrinol Metab 299: E808-815 (2010)
  4. Yeboah J, Crouse JR, Hsu FC, Burke GL, and Herrington DM. “Brachial flow-mediated dilation predicts incident cardiovascular events in older adults.” J Am Coll Cardio 51: 997-1002 (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.