Archive for February, 2012

Confessions of a Wheat Addict

Saturday, February 18th, 2012

Confessions of a Wheat Addict

Ever since learning how wheat causes gut inflammation in nearly everyone, I came to terms with the fact that I have no room in my life for wheat, or any cereal grains, since I have a history of digestive disorders. After being a regular pasta junkie for the better part of my life, I quit. Cold turkey. 3 weeks ago. The great news is how much more mental clarity I have with the lifting of persistent “brain fog” that I couldn’t put my finger on.

But guess what? Those wheat-derived opioids are real: nausea, muscle tension in my TMJ, lightheadness, fatigue. I am in the middle of wheat withdrawal.

What gives? At first, this seemed ridiculous but after Googling “wheat withdrawal”, it became clear that many people experience this short-term setback for the long-term benefit of eliminating wheat from their diets.  Like celiacs or others with leaky gut, I crave the very food that makes me predisposed to illness: wheat. Eliminating corn (apparently a close second to wheat in toxicity) has been comparatively easy. While I miss the idea of corn chips with salsa and guacamole or polenta with homemade chicken cacciatore, I don’t crave it the way I do a plate of fresh pasta with homemade Bolognese sauce right after a long day of skiing. Little did I realize that my narcotic habit was in the form of food.

Wheat poses a double-whammy: it is toxic due to its gluten, wheat germ agglutinin, and opioid content (see blog entry, “The Controversy of Wheat (and all cereal grains for that matter …”), and it contributes to excessive carbohydrate intake (see last week’s blog, “Carbohydrates: The Smoking Gun?”).

In replacing wheat with other more favorable foods, I am concerned about 1) fiber, 2) minerals and vitamins, and 3) “safer” sources of carbohydrates.  My big picture is also transitioning to a different macronutrient profile, i.e., less carbs, less protein, and higher consumption of healthy fats, that is tailored to what works best for me (for more information, read “Perfect Health Diet” by Jaminet and Jaminet).

The opportunity of subtracting toxic foods from one’s diet is discovering new foods that are more satisfying to eat, make you feel good, and contribute to long-term health and vitality. Truly, the opportunity is to find ways to enjoy your dietary changes.

For instance, I eat greens and vegetables in much greater quantities than before, including sauteed kale with shitake mushrooms, salad, homemade fermented foods like vegetable medleys (e.g., cauliflower, carrots, celery, with jalapeno) and sauerkraut. I eat in lesser quantities “safer” starches such as rice, sweet potatoes, yams, and starchy vegetables like carrots and squash. More than ever, healthy sources of fat, such as Melt® Organic, organic goat milk kefir, sheep’s milk cheese (e.g., Manchego), pastured organic eggs, avocados, and virgin coconut oil are critical for stabilizing my blood sugar and fueling my daily work and sports activities.  While I am a believer and huge fan of virgin coconut oil, I find Melt® Organic to be a much more versatile and flavorful way of getting my MCFAs and my Omega 3s all at once. I love adding a dollop of Melt® Organic on grilled steak, salmon, or scallops.

The essence of nutritional therapy is buying into the concept that diet is the foundation of health or disease.  Not even exercise can trump this underlying reality, though it can postpone some of the effects of an unconscious diet. This can at first be demoralizing, given the high degree of confusion in nutritional “expertise”. However, it is far more empowering to control your own destiny in regards to your health even if it means wading through the lack of consensus.

As for me, experiencing symptoms of wheat withdrawal helps me tap into my determination to ride it out for a happier, healthier life.

–Cygnia F. Rapp, Founder of Prosperity Organic Foods.

 

Carbohydrates: The Smoking Gun?

Wednesday, February 8th, 2012

Carbohydrates: The Smoking Gun?

This week’s blog follows on last week’s blog entry, “The Controversy of Wheat (and all cereal grains for that matter…)”, by discussing the serious concerns around high-carb diets and currently held ideas of appropriate carbohydrate intake. This is within the backdrop of the USDA’s recently revised dietary guidelines that recommends children, adolescents, and adults consume an astonishing 45-65% of their calories in the form of carbohydrates. The USDA’s recommendation for dominating one’s diet with carbohydrates is directly counter to mounting evidence that carbohydrate (not fat) intake beyond low- to moderate-amounts is quite possibly a causal factor for obesity, metabolic syndrome, cardiovascular disease, and other serious conditions (e.g., Siri-Torino et al., 2010 a&b; Hite et al., 2010; Micha and Mozaffarian, 2010; Jaminet and Jaminet, 2010).

Carbohydrate intake requirements vary depending on age and activity level; for example, breast milk offers infants 40% carbohydrates to support rapid brain development and growth. However, as a nation reared on grains we need to take a step back and understand the risks of a high-carb diet. The amount of carbohydrates one should consume for optimal health is a highly controversial topic, but at its heart underscores how important glucose is as a nutrient, which can be manufactured from fat and protein as well as from carbohydrates.

Why We Need Glucose

Most plant foods are broken down in the digestive tract to indigestible fiber or to simple sugars glucose and fructose.

Potentially useful carbs are those that digest to glucose or galactose, such as starch and milk sugars, and indigestible fiber that feeds gut bacteria. According to Jaminet and Jaminet (2010), fructose is potentially toxic at any level because it reacts with proteins and creates toxins. In order to prevent this “fructation”, the body shunts fructose to the liver for disposal where it is most likely to be converted to fat. Since the conversion process damages the liver, moderate- to high-levels of fructose in the diet potentially lead to metabolic syndrome.

How Much Glucose Does the Body Need?

Glucose has three main uses in the body:

  • Combines with proteins to form structural molecules called glycoproteins;
  • Serves as an alternate fuel that cells can burn instead of fats; and
  • Is a precursor for killing compounds (“reactive oxygen species” or ROS) made by immune cells.

A fasting person’s daily glucose production is around 120-160 grams or 480-640 calories per day (Nair et al., 1987).

Glucose in structural molecules: Some structural sugar compounds are highly abundant in the body such as mucin, which is one of the main components of mucus, and protects the gut and airways from pathogens and foreign matter. It is also a key part of tears and saliva. Hyaluronan lubricates joints and helps provide the scaffolding that shapes cells into tissues. Glucosamine and chondroitin sulfate are similar sugar-rich compounds important in connective tissue (Jaminet and Jaminet, 2010).

Glucose as fuel for neurons: One often hears that glucose is the body’s “primary fuel”. This is quite mistaken. While it is true that all human cells can, if needed, metabolize glucose, mitochondria (the energy producers in most human cells) prefer to burn fat. In the body, fat is the preferred and primary fuel except in specialist cells that lack mitochondria (red blood cells) or avoid fat metabolism (neurons). Normal glucose-as-a-fuel consumption is dominated by neurons. The brain and nerves require about 20 calories per hour, waking or sleeping. These 480 daily calories can be provided by either glucose alone or a mix of glucose and ketone bodies (derived from fats or protein). Daily glucose consumption by the brain and nerves is somewhere between 150 to 480 calories depending on ketone availability (Jaminet and Jaminet, 2010).

Glucose for muscle glycogen: Muscles consume glucose in the form of glycogen during intense exertion. Muscle glycogen usage is a relatively small drain on glucose. Highly trained runners use about 50 glycogen calories per mile. Highly trained cyclists cycling at 70% of maximum oxygen utilization (an intense pace) use about 500 calories of glycogen per hour. Low intensity exercise for shorter periods of time (which is most of us) require very few extra glucose calories to maintain muscle glycogen levels. Someone who exercises 20 minutes per day at moderate intensity probably uses less than 50 glycogen calories (Jaminet and Jaminet, 2010).

Glucose as a killing agent: One reason most cells prefer fats to glucose as an energy source is that fats burn cleanly while glucose, when metabolized for energy, produces reactive oxygen species (ROS). ROS are dangerous molecules that can damage or destroy cells. The destructiveness of ROS is used by the immune system with immune cells called macrophages that create and use ROS to kill pathogens like bacteria and fungi. Under normal circumstances the immune system does not consume much glucose for killing pathogens, however people with chronic infections, especially fungi or protozoa, may need extra glucose (Jaminet and Jaminet, 2010).

Endogenous glucose production: Glucose is also routinely produced by the body as a consequence of metabolizing fats. Fats are stored in the body as either phospholipids, which consist of two fatty acids joined by a glycerol backbone to a phosphate group and an organic molecule like choline or inositol, or triglycerides, which consist of three fatty acids and a glycerol backbone. Phospholipids make up cell membranes, while triglycerides are a storage form of fats. When fatty acids are consumed for energy, the glycerol backbones are released. Two glycerols make one molecule of glucose. Recycling of glycerol from fats helps to meet the body’s glucose needs, since fats in food enter the body already attached to glycerol backbones. A typical triglyceride provides about 12% of calories as glycerol, 88% as fatty acids (Jaminet and Jaminet, 2010).

Although the precise number for glucose requirements remains uncertain, it appears the body needs about 150-480 calories for the brain and nerves, 200-300 calories for glycoproteins such as mucin, and 100 calories for muscle glycogen and immune, intestinal, and kidney cell use, some of which is offset in the course of burning fat. In elite athletes, glucose needs are increased by 50 to 100 calories per hour of training. For most people, around 400-650 daily glucose calories must be obtained from the diet, manufactured from protein, or replaced with ketones (Jaminet and Jaminet, 2010).

Risks of Too Much Glucose

Two sources of damage occur from eating excessive carbohydrates and include:

  • Hyperglycemia (“too much sugar”), sugar poisoning that inflicts damage, and
  • Hyperinsulinemia (“too much insulin”), insulin, a hormone that helps dispose of excess glucose, and inflicts damage by hastening aging, weakening defenses against infection, hardening the arteries, and impairing the mind.

Glucose in excess of bodily needs has toxic effects and ruins health. For purposes of this discussion (i.e., length considerations) we focus on the toxic effects of hyperglycemia, which is adapted from Jaminet and Jaminet (2010).

Ideally, blood glucose levels should remain in a stable range between about 85 to 105 mg/dl. After eating carbohydrates blood glucose typically rises into the 120s to 140s and fall back to the normal range in a few hours. As people increase carb consumption above the body’s glucose needs, they become reliant on slow disposal mechanisms like fat formation and average blood glucose levels go up. If the liver and pancreas are poisoned by toxins like fructose, omega-6 fats, and wheat, insulin resistance may develop and blood glucose levels rise even further.

Dietary carbs cause the atherogenic blood lipid profile: While its well known that a bad lipid profile (high triglycerides, low HDL, high levels of “small, dense” LDL) is a risk factor for heart disease, it is less commonly appreciated that the bad blood lipid profile is almost entirely determined by excess carbohydrate consumption. A series of studies by Dr Ronald Krauss grouped people by the carbohydrate fraction of their diet and measured their blood lipids, classifying them as “atherogenic” or “non-atherogenic”. A slide show by Dr Krauss illustrating this phenomenon can be viewed here: http://www.ciaprochef.com/wohf2009/presentations/RONALD_KRAUSS_Healthy_Metabolism.pdf. The results of the study (Krauss, 2001) suggest that atherogenic lipid profiles may disappear with carb consumption of 25% of energy or less. Any carb intake above this level has to be disposed of, ideally through fat conversion; while this disposal takes place, glucose levels are unnecessarily elevated and glucose toxicity damages health.

Nerve damage occurs when blood sugars rise over 140 mg/dl: In a study of patients with peripheral neuropathy of unknown origin, neurologists found that many people who don’t have diabetes nevertheless have “diabetes neuropathy”, nerve damage from excess glucose. Moreover, when given a glucose tolerance test, the degree to which blood sugars rose over 140 mg/dl was correlated with severity of the neuropathy (Singleton et al., 2001). Since most people’s blood sugars rise over 140 mg/dl after a carb-rich meal, this suggests that most people may be poisoning their nerves incrementally every day. The MONICA study showed that 13% of non-diabetics whose blood sugar rises over 140 mg/dl after a carb-rich meal have nerve damage.

Hyperglycemia destroys the organs of diabetics: In diabetics, organ damage arises from glucose toxicity, primarily due to uncontrolled glycation of proteins by excess blood sugar (Rossetti, 1999; Mooradian and Thurman, 1999). Elevated blood glucose causes neuropathy (nerve damage), nephropathy (kidney damage), retinopathy (eye damage), and cardiovascular disease (The Diabetes Control and Complications Trial Research Group, 1993; UK Prospective Diabetes Study Group, 1998).

Hyperglycemia increases mortality: “Hemoglobin A1c” or HbA1c is useful for measuring average blood glucose levels over the past 30 days. HbA1c measures how much of the hemoglobin on red blood cells is glycated. It is possible to achieve HbA1c levels below 5%, but many people on high-carb diets develop HbA1c levels above 7%. HbA1c is an index of glucose poisoning. The EPIC (European prospective investigation into cancer) study measured HbA1c values in 4462 men and 5570 women aged 45 to 79, and then followed patients, tracking death rates for an average of 6 years (Khaw et al., 2004). They found that men with HbA1c levels above 7% were 5 times more likely to die than men with HbA1c levels below 5%. Women with higher HbA1c values were 12.5 times more likely to die, mostly from heart disease. The risk of heart attacks was increased 7.5-fold in men and 9.5-fold in women by high HbA1c. Blood sugar levels were a strong indicator of heart disease risk. If you want to avoid a heart attack, keep blood sugar low.

Blood glucose levels determine stroke risk: The Whitehall study gave a glucose tolerance test to 19,019 men and then tracked their mortality for 38 years. The risk of stroke rose in a linear fashion with blood glucose level 2 hours after consuming 50 g (200 calories) of glucose. Stroke mortality was lowest with a reading of 83 mg/dl. For every 18 mg/dl above that level, there was a 27% increase in stroke mortality (Batty et al., 2008).

Dietary carbs and heart attacks: Since the EPIC study showed that blood glucose levels, indicated by HbA1c, are responsible for most cardiovascular disease, one would think there is an association between high-carb diets and cardiovascular disease. This question was investigated by a mammoth long-term US study, the Nurse’s Health Study. A 2006 report in the New England Journal of Medicine summarized the effects of carbohydrate composition on the nurses health (Halton et al., 2006). The researchers followed 98,462 women who completed a 1980 diet questionnaire, and split the women into ten equal-sized groups based on the fraction of calories obtained from carbohydrates. For simplicity, the bottom decile obtained 58.8% of calories from carbs and 26.9% from fat (the “high-carb group”); the top decile obtained 36.8 of calories from carbs and 39.9% from fat (the “moderate-carb group”). In general, the moderate-carb group did not take good care of their health: they smoked (26% smoked, compared to 17% in the high-carb group), avoided exercise (20% less exercise than the high carb group), and they drank a lot of coffee. However, the chances of a heart attack in the high-carb group was 42% higher than the moderate-carb group who smoked more and exercised less.

Hyperglycemia worsens the outcome of every health condition: Similar to EPIC patients, critically ill patients in hospitals are more likely to experience death the higher the blood glucose levels, no matter what the health problem. More importantly, lowering blood glucose reduces the chance of death or poor outcome. To summarize, high blood glucose levels have been associated with morbidity and poor outcome in critically ill patients, irrespective of underlying pathology. In a large, randomized controlled study the use of insulin therapy to maintain normoglycemia for at least a few days improved survival and reduced morbidity of patients who are in surgical intensive care unit (Vanhorebeek and Langouche, 2009). Hyperglycemia is a common feature of the critically ill and has been associated with increased mortality. Maintaining normoglycemia with intensive insulin therapy improves survival rates and reduces morbidty in prolonged critically ill patients in both surgical and medical intensive care units, as shown by 2 large randomized controlled studies (Vanhorebeek et al., 2006). These trials reduced blood glucose with drugs. A low-carb diet may have reduced blood glucose without drugs, and possibly produced better results.

Hyperglycemia promotes bacterial infections and many diseases: Chronic infections with parasitic bacteria aggravate or cause a host of diseases. The parasitic bacteria Chlamydophila pneumoniae has been associated with cardiovascular disease, Alzheimer’s. multiple sclerosis, arthritis, and rosacae. The bacterial genus Nocardia has been associated with Parkinson’s, and Borrelia burgdorferi with Lyme disease. Chronic fatigue appears to be caused by Human Gamma Retrovirus. Most chronic diseases, including autoimmune diseases, are probably caused by parasitic, bacterial, viral, or protozoa infections. Bacteria cannot use fats for fuel. They are dependent upon glucose and its metabolites like pyruvate and lactate. Hyperglycemia delivers more glucose into cells, enabling parasitic bacteria to feed and multiply.

Hyperglycemia promotes cancer progression: Cancer cells, like bacteria cannot burn fats. If mitochondria in cancer cells are allowed to burn fats the cell dies. Cancer cells are dependent on glucose for energy, known as the Warburg Effect. Higher blood glucose levels provide more fuel to tumor cells, stimulate their proliferation, and hasten the progression of cancer. If high blood glucose induces cells to start burning glucose, it may actually cause cancer by switching them from normal metabolism to tumor cell metabolism. A Swedish study followed 64,597 people for 10 years and found that people who had fasting blood sugars over 110 mg/dl or who scored over 160 mg/dl two hours after a glucose tolerance test has much higher rates of cancer. The cancers most frequently induced by high blood sugars were cancers of the pancreas, endometrium, urinary tract, and malignant melanoma (Stattin et al., 2007). In contrast, ketogenic diets which keep blood glucose levels low and provide keton bodies to mitochondria have shown remarkable effectiveness at slowing cancer progression. In vitro, ketone bodies have been shown to sometimes restore mitochondria to health, triggering cancer cell death. Ketogenic diets have been shown in clinical trials to slow the progress of brain cancer, and clinical trials for other cancers are in progress. In short, keeping blood glucose levels low, and mixing in some ketone bodies, may help prevent cancer or slow the progression of established cancers.

The Bottom Line

Find your own “sweet spot” for reducing total carbohydrate intake. Adjusting carbohydrate intake is an individual journey that requires personal experimentation and listening to your body for feedback on whether the approach you have chosen is right for your unique biochemistry and genetics. Achieving the goal of optimal health is only possible when you listen to that feedback and adjust your program accordingly.

Defining appropriate carbohydrate intake is controversial and is not “one size fits all”. Some, such as Dr Rosedale, recommend a diet dominated by healthy fats and protein (including those found in organ meat) with carbohydrates restricted to less than 20% of total dietary intake. While this approach may work amazingly well for some, for others this could be too extreme and could pose problems due to glucose deficiency. It may also be an unrealistic goal for many.  Others, such as Dr Jaminet, are a little more forgiving by recommending 20-25% carbohydrate intake with the remaining calories from mostly healthful fats (60-65%) and secondarily from protein (15%). His recommended sources of “safe” carbohydrates are starchy foods like potatoes, taro, sweet potatoes, yams, rice, and starchy vegetables like carrots and squash. Non-starchy vegetables (e.g., dark leafy greens) have a “free pass” and can and should be eaten as much as desired. Grains and legumes are avoided entirely.  For further information, you can read an on-going debate between Dr Rosedale and Dr Jaminet: Perfect Health Diet: Safe Starches Symposium.

Personally, I plan on experimenting with reducing total carbohydrate intake to 30% to see what happens. Since I am a moderately active, athletic person, I am concerned about reducing my carbohydrate intake to less than 30%. I also feel this goal is more achievable.

Consume non-toxic forms of carbohydrates. Regardless of the carbohydrates you choose to include in your meals, finding organic, un-processed sources are important to ensure they are free of pesticides, GMOs, and chemical additives and retain maximum nutrient levels.

Some who have given up grains entirely have thrived; others found they had nutritional deficiencies that were reversed when they re-introduced grains using appropriate methods to detoxify them (i.e., fermentation). Safer methods for consuming whole grains and legumes include soaking grains (including brown rice) for at least 24 hours in advance of cooking using whey, vinegar, or lemon juice. Fermentation and soaking reduce the toxicity of protein compounds discussed in last week’s post, “The Controversy of Wheat (and all cereal grains for that matter)”. The Weston Price Foundation provides information on techniques for reducing these toxic compounds, which they refer to as “anti-nutrients”. Sprouted grain products are also another option; sprouted grains reduce the toxicity of these protein compounds, but may not eliminate them entirely.

Most importantly, enjoy your food and your health!

–Cygnia F. Rapp, Founder of Prosperity Organic Foods

References

Batty GD et al. 2008. Post-challenge blood glucose concentration and stroke mortality rates in non-diabetic men in London: 38-year follow-up of the original Whitehall prospective cohort study. Diabetologia 51(8):1123-6.

Halton TL et al. 2006. Low-carbohydrate-diet score and the risk of coronary heart disease in women. N Engl J Med 355(19):1991-2002.

Hite AH et al. 2010. In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee. Nutrition 26:915–924.

Jaminet P, Jaminet SC. 2010 Perfect Health Diet.YinYang Press, Cambridge, MA.

Khaw KT et al. 2004. Association of hemoglobin A1c with cardiovascular disease and mortality in adults: the European prospective investigation into cancer in Norfolk. Ann Intern Led 141(6):413-20.

Krauss RM. 2001. Atherogenic lipoprotein phenotype and diet-gone interactions. J Nutr 131(2):340S-3S.

Micha R, Mozaffarian D. 2010. Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence. Lipids 45:893-905.

Mooradian AD, Thurman JE. 1999. Glucotoxicity: potential mechanisms. Clin Geriatr Med 15(2):255.

Nair KS et al. 1987. Leucine, glucose, and energy metabolism after 3 days of fasting in healthy human subjects. Am J Clin Nutr 46(4):557-62.

Rossetti L. 1995. Glucose toxicity: the implications of hyperglycemia in the pathophysiology of diabetes mellitus. Clin Invest Med 18(4):255-60.

Singleton JR et al. 2001. Increased prevalence of impaired glucose tolerance in patients with painful sensory neuropathy. Diabetes Care 24(8):1448-53.

Siri-Tarino P et al. 2010a. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J of Clin Nutr 91:535-46.

Siri-Tarino P et al. 2010b. Saturated fat, carbohydrate, and cardiovascular disease. Am J of Clin Nutr 91:502-9.

Stattin P et al. 2007. Prospective study of hyperglycemia and cancer risk. Diabetes Care 30(3):561-7.

The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 329(14):977-86.

UK Prospective Diabetes Study (UKPDS 33) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 352(9131):837-53.

Vanhorebeek I et al. 2006. Intensive insulin therapy in the intensive care unit: update on clinical impact and mechanisms of action. Endocr Pract 12 Suppl 3:14-22.

Vanhorebeek I, Langouche L. 2009. Molecular mechanisms behind clinical benefits of intensive insulin therapy during critical illness: glucose versus insulin. Best Pract Res Clin Anaethesiol 23(4):449-59.