American Sugar: The Untold Story.

There is a metabolic difference between simple and complex carbohydrates. The simple ones become glucose soon after they are eaten. The complex ones take longer to turn into sugar and are less apt to spike insulin and cause energy crashes down the line. But that isn’t the only difference between the two.

Almost forty years ago scientists had an interest in the relationship of diet to health, specifically of sugar intake to immunity. But their curiosity went past simple sugar to include carbohydrates other than glucose. The cells that are the backbone of the immune system are supposed to kill, swallow, and dispose of alien bodies, including bacteria, viruses and cancer cells. Scientists at Loma Linda University in California examined the activity of neutrophilic phagocytes (cells that dissolve the enemy) after subjects ingested glucose, fructose, sucrose, honey, or orange juice and found that “…all significantly decreased the capacity of neutrophils to engulf bacteria…” (Sanchez, Reeser, et al. 1973). Looking more closely, the researchers also discovered that the greatest effects occurred within the first two hours after eating, but “…the effects last for at least 5 hours.” (Ibid.) If there is any promise, it’s that the effects can be undone by fasting from added sugars for the next two or three days.

At the start of the twentieth century, Americans consumed only about five pounds of sugar a year. By the fifties, that had grown to almost 110 pounds a year, and to more than 152 by the year 2000. Corn sweeteners account for 85 of those pounds. America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the statistics above are decades old, its message is contemporary. High-fructose corn syrup has become the bad boy of the anti-sugar crusade. HFCS began replacing sugar in soft drinks in the 1980’s, after it was portrayed by marketers as a healthful replacement for demon sugar. It didn’t hurt the industry that it cost less, either. The biological effects of sugar and HFCS are the same, however. Neither has any food value — no vitamins, protein, minerals, antioxidants, or fiber — but they do displace the more nutritious elements of one’s diet, and we tend to consume more than we need to maintain our weight, so we gain.

Even though the number of calories from the glucose in a slice of bread or other starch is the same as that from table sugar (half fructose and half glucose), they are metabolized differently and have different effects on the body. While fructose is metabolized by the liver, glucose is metabolized by every cell in the body. When fructose reaches the liver, especially in liquid form (as in soda), it overwhelms the organ and is almost immediately converted to fat. (Taubes. 2011)

Innate immunity is that which occurs as part of your natural makeup and defends you against infection by other organisms. Short-term hyperglycemia, which might come from a pint of vanilla, has been found to affect all the major components of the innate immune system and to impair its ability to combat infection. Reduced neutrophil activity, but not necessarily reduced neutrophil numbers, is one of several reactions to high sugar intake. (Turina. 2005) Way back in the early 1900’s, researchers noted a relationship between glucose levels and infection frequency among diabetes sufferers, but it wasn’t until the 1940’s that scientists found that diabetics’ white cells were sluggish. (Challem. 1997) More recent study has corroborated the diabetes-infection connection, agreeing that neutrophil phagocytosis is impaired when glucose control is less than adequate. (Lin. 2006) Impaired immune activity is not limited to those with diabetes. As soon as glucose goes up, immune function goes down.

Some people think they’re doing themselves a favor by using artificial sweeteners. Once the brain is fooled into thinking a sweet has been swallowed, it directs the pancreas to make insulin to carry the “sugar” to the cells for energy. After the insulin finds out it’s been cheated of real sugar, it tells the body to eat in order to get some, and that creates artificial hunger, which causes weight increase from overeating. Even environmental scientists have a concern with fake sweeteners in that they appear in the public’s drinking water after use. You can guess how that works. (Mawhinney. 2011)

Mineral deficiencies, especially prevalent in a fast-food world, contribute to immune dysfunction by inhibiting all aspects of the system, from immune cell adherence to antibody activity. Paramount among minerals is magnesium, which is part of both the innate and acquired immune responses. (Tam. 2003) Epidemiological studies have connected magnesium intake to decreased incidence of respiratory infections (PDR. 2000). But sugar pushes magnesium — and other minerals — out of the body. (Milne. 2000) This will compromise not only immune function, but also bone integrity. (Tjäderhane. 1998). Mix a sweet alcohol cocktail and find the whammy doubled. (Fuchs. 2002).

Zinc has been touted for its ability to shorten the duration of the common cold. Like magnesium, zinc levels decrease with age, and even tiny deficiencies can have a large effect on immune health, particularly in the function of the thymus gland, which makes the T-cells of the immune system. Zinc supplementation improves immune response in both the young and the old. (Haase. 2009) (Bogden. 2004) (Bondestam. 1985) All the microminerals, in fact, are needed in minute amounts for optimal growth and development…and physiology. Low intakes suppress immune function by affecting T-cell and antibody response. Thus begins a cycle whereby infection prevents uptake of the minerals that could prevent infection in the first place. Adequate intakes of selenium, zinc, copper, iron plus vitamins B6, folate, C, D, A, and E have been found to counteract potential damage by reactive oxygen species and to enhance immune function. (Wintergest. 2007)

Who would have viewed something as sweet as sugar as being so hostile to its host? It likes to let itself in, but has the nasty character of pushing everything else out.

Reference

Albert Sanchez, J. L. Reeser, H. S. Lau, P. Y. Yahiku, et al. Role of sugars in human neutrophilic phagocytosis. American Journal of Clinical Nutrition, Nov 1973; Vol 26, 1180–1184

Profiling Food Consumption in America. USDA http://www.usda.gov/factbook/chapter2.pdf

Taubes G. “Is Sugar Toxic?” in New York times Magazine, 13 April, 2011

Turina M, Fry DE, Polk HC Jr. Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects. Crit Care Med. 2005 Jul;33(7):1624–33.

Challem J and Heumer RP. The Natural health Guide to Beating the Supergerms. 1997. Simon and Schuster Inc. New York. Pp. 124–125

Lin JC, Siu LK, Fung CP, Tsou HH, Wang JJ, Chen CT, Wang SC, Chang FY. Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella pneumoniae in type 2 diabetes mellitus patients with poor glycemic control. J Clin Endocrinol Metab. 2006 Aug;91(8):3084–7.

Mawhinney DB, Young RB, Vanderford BJ, Borch T, Snyder SA. Artificial sweetener sucralose in U.S. drinking water systems. Environ Sci Technol. 2011 Oct 15;45(20):8716–22.

Tam M, Gómez S, González-Gross M, Marcos A. Possible roles of magnesium on the immune system. Eur J Clin Nutr. 2003 Oct;57(10):1193–7.

PDR: Physicians’ Desk reference for Herbal Medicines. Magnesium. 2nd edition. Mintvale NJ: Medical Economics Company; 2000: 5340540

Milne David B, PhD and Forrest H. Nielsen, PhD. The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men. J Am Coll Nutr February 2000 vol. 19 no. 1 31–37

Tjäderhane Leo, and Markku Larmas. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. J. Nutr. October 1, 1998 vol. 128 no. 10 1807–1810

Fuchs, Nan Kathryn Ph.D. Magnesium: A Key to Calcium Absorption. The Magnesium Web Site on November 22, 2002. http://www.mgwater.com/calmagab.shtml

Haase H, Rink L. The immune system and the impact of zinc during aging.. Immun Ageing. 2009 Jun 12;6:9.

Bogden JD.. Influence of zinc on immunity in the elderly.. J Nutr Health Aging. 2004;8(1):48–54.

Bondestam M, Foucard T, Gebre-Medhin M. Subclinical trace element deficiency in children with undue susceptibility to infections. Acta Paediatr Scand. 1985 Jul;74(4):515–20.

Wintergerst ES, Maggini S, Hornig DH. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 2007;51(4):301–23. Epub 2007 Aug 28.

Smolders I, Loo JV, Sarre S, Ebinger G, Michotte Y. Effects of dietary sucrose on hippocampal serotonin release: a microdialysis study in the freely-moving rat. Br J Nutr. 2001 Aug;86(2):151–5.

Jack Challem, Burton Berkson, M.D., Ph.D., Melissa Diane Smith Glucose and Immunity http://www.diabeteslibrary.org/View.aspx?url=Article638 Accessed 11/2011

Van Oss CJ. Influence of glucose levels on the in vitro phagocytosis of bacteria by human neutrophils. Infect Immun. 1971 Jul;4(1):54–9.

Bernstein J, Alpert S, et al Depression of lymphocyte transformation following oral glucose ingestion. Am J Clin Nutr. 1977; 30: 613

Robert A. Good, Ellen Lorenz. Nutrition and cellular immunity. International Journal of Immunopharmacology. Vol 14, Iss 3, Apr 1992, Pp. 361–366

A Professional Athlete on Nutrition

‘Recovery’ is the focal point of my last post, but this week I’ll delve into nutritional strategies in the life of an elite endurance athlete. It’s safe to say that nutrition and energy availability play a significant role in adaptation, growth and success in preparation for performance. Without the proper nutritional and supplemental intake, an athlete can become vulnerable to injury, illness and counteract all the hard work put into a specific training session or cycle.

I recently learned that this was, in fact, one of the possible contributing factors to my recent diagnosis of a stress fracture. My nutritional support team had a look at two-weeks’ worth of food intake aligned with training sessions and found that I was operating in a deficit. Although I generally felt that I was getting in enough carbs, proteins, fats, etc., it turned out that I was continually missing the mark to offset the physical demands and training loads. The deficit may have been small at the end of the day, but over time, all those days add up to a larger, more impactful loss. Take a look at this food-log example pre-stress fracture:

Although this generally meets most daily nutritional needs, it still does not cover the calories burned over the course of a 4.5–5-hour training day in addition to the calories burned by my resting metabolic rate. Doubling the amount of sports drink, upping the morning orange juice, and adding in a peanut-butter & jelly sandwich or cereal bar mid-ride are all strategies to help offset some of the deficit and actually help the body recover quicker for the next session on tap. And while a PB&J might not be the ideal food for a non-endurance athlete, I often rely on these foods because of how easy they convert to sugar and energy during a training session.

Likewise, it’s also important to consider supplement value-adds for optimal vitamin absorption. As a female endurance athlete, iron, vitamin C and vitamin D are some of the most foundational to maintain health under training stress. I also find Calcium and BodyBio’s PC to be valuable in enhancing my bone and cellular regeneration, especially in recovery from injury. It’s challenging to get all of the nutrients and energy in during a day so I find it helpful with some assistance by trusted supplements.

Timing of intake, nutrient density foods, supplements and flexibility around managing food strategies are all key components in the creation of a healthy, balanced & fortified diet as an elite athlete. It’s important to alter your diet relative to the physical demands of the day — whether you’re an athlete, working a desk job, or an active retiree. I know I’m continually working on improving my strategies in order to optimize those 1%-ers that make all the difference in performance on the day. And I’m a strong believer that everyone can do the same in order to optimize those 1%-ers in life!

What is a Liposome?

(lĭp′ə-sōm′, lī′pə-)

Not discernable with a light microscope, a nanoliposome can be seen under an electron microscope as a sphere. Just as a water balloon has a thin outer layer with a water-filled interior, a liposome likewise has a thin outer wall — similar to a membrane — made of a phospholipid bilayer and an interior containing a water-soluble material. First identified in the early 1960’s, liposomes have undergone extensive research, the aim being the optimization of encapsulation, stability, circulation time and targeted delivery of its cargo, which may be a drug or a nutrient to a specific site of action. Until recently, the use of liposomes as a carrier of nutriments was limited, the delivery of drugs being more the focus. Their versatility is now being realized in other domains.

A few companies are pioneering the benefits of this unique science. It has long been the case that absorption and bioavailability rates of oral dietary and nutritional tablets and capsules is low and unreliable. Now, the natural encapsulation of lipophilic and hydrophilic nutrients within a liposome has created an effective method of bypassing the destructive elements of the digestive system, allowing the encapsulated nutrient to be delivered directly to cells and tissues.

To make a suitable microscope image, the liposomes are frozen and then sliced into ridiculously thin layers. This “freeze fracturing” will open some, but not all, and you will be able to distinguish the intact spheres from the concave surfaces of the incised liposomes. If this arrangement fails to emerge, you most likely do not have liposomes. But most clinics and manufacturers do not own electron microscopes. So, how do you determine that you have liposomes? Mix your material with water. Solid globs of amorphous matter are not carrying anything inside them and are not liposomes. If this happens, the phosphatidylcholine (PC) content is either too low, of poor quality, or is non-existent. If what you think is a liposome appears to be floating in foam, you are stuck with a mere emulsion, not a liposome. The liquid around a liposome should be clear.

Liposomes do not form spontaneously, typically needing energy applied to a dispersion of PC in a polar solvent, such as water. Heat, agitation and the aqueous province of the human body afford the right conditions. Sonication of phospholipids in water does the same thing, but likely will form layers like those of an onion, with progressively smaller liposomes. The inclusion of ancillary lipids facilitates the preparation. Microscopic vesicles — nanoliposomes — of PC can trap desirable payloads and provide controlled release of various bioactive agents at the right place at the right time. Here, otherwise volatile, reactive or sensitive additives become stabilized. Liposomes are bioresponsive because they and cell membranes share a common constituent — the lipid bilayer. As liposomes and cell membranes sidle near each other, they become conjugated and meld into each other, allowing the liposomal cargo to be deposited in the cellular cytosol, where its ameliorative destiny can be fulfilled. Liposomes with target specificity offer the prospect of safe and effective therapy for challenging clinical uses.

A Professional Athlete’s Road to Recovery

Hey everyone, Renée Tomlin here to talk about ‘recovery’. For a bit of background information, I’m a professional triathlete and member of Team USA in international competition. I’ve been competing in triathlon since 2014 with an Olympic focus, and ran competitively in college and at the elite level before moving over to endurance multisport. I’m fortunate to live, train and compete all over the world representing the USA.

So, you might be wondering what my background has to do with ‘recovery’. Well, quite simply, I wouldn’t be able to do my job — compete and execute performance — without the proper tools in my recovery tool box. Generally speaking, I’m out training 7 days a week, usually clocking 20–28 hours of exercise at various volumes and intensities. Between swimming, biking, running and gym work, recovery is the most crucial component in creating fitness, competitive edge and in maintaining health. For me, recovery includes nutrition, sleep, physical and massage therapy, hormone balance and the ‘switch off’ of all things triathlon.

In terms of nutrition, I’ve recently started working with a specialist from my Australian support team on strategies to maximize my training gains through food and energy availability. Having an understanding of carbs, protein, calcium, electrolytes, (just to name a few) plays a significant role in optimizing a nutrition plan to match the demands of training and competition. As an elite athlete, it’s challenging to keep up with all of stressors placed on your body — and that’s why I rely on vitamins like iron, vitamin C, and vitamin D to contribute to my nutritional intake. Sports drinks that contain carbs are also essential, as well as sport-specific electrolyte drinks, like Elyte-Sport, for pre-loading or between sessions. Both supplements and sports drinks act as ancillary agents in encouraging my body to prepare for training demands, recover from them, and foster training adaptations. They directly impact energy levels, nutritional absorption and healthy blood counts.

True life confession: it’s impossible as a professional athlete to always maintain an optimal level of ‘recovery’ as you’re always pressing physical and mental boundaries. Somewhere along the way you slip — that’s called being human. Just this past week I was diagnosed with a navicular stress fracture, barring me from early competition and resulting in a quick return back to the US for doctor appointments and to start, yes, in broader terms, the ‘recovery’ process. Now just as ever does ‘recovery’ play a significant role in achieving future goals. Fortunately, I have an incredible support team behind me in outlining these next-steps, many of which include a re-evaluation of nutrition and supplement intake. That being said, recovery — specifically in the field of nutrition and supplements — is an evolving space. As the body changes, grows, ages, heals, dietary requirements can shift. Stay tuned for an update of what this unfolding recovery process looks like and what tweaks are made!

Follow Renee’s journey on Twitter @ReneeTomlin

No “Bones” About It…

Essential Fatty Acids and BonesEssential Fatty Acids may be a key ingredient in supporting bone health.

Essential fatty acids (EFAs) do not come to mind as the first thought in searching for nutritional answers regarding bone health.  “Recent evidence-based research, however, supports intervention with adequate amounts of specific nutrients including vitamin D, strontium, vitamin K, and essential fatty acids in the prevention and primary management of osteoporosis” (Genius, Clin Nutr. 2007).  Osteoporosis has become an epidemic in the Western World in recent years.  How do EFAs fit into this problem that plagues us especially as we get older?

When we think about osteoperosis, we think calcium.  Calcium and bone go together like salt and pepper.  Add in some vitamin D and that’s about it.  However, looking into it deeper we came up with a number of studies that say that EFAs should be right up front and strongly considered in our first line of bone defense.

Essential fatty acids are necessary to human survival, and are called essential because they must come from the diet; they cannot be made by the body.  The omega-6 and omega-3 fatty acids are the best known.  Learning that they are also important for bone health is something we need to know.

In vivo studies (that means in a living animal) have shown that supplementation with long chain n-6 poly-unsaturated fatty acids (PUFAs) in rats causes increases in intestinal Calcium absorption (Haag 2001).  Haag and his colleagues reported a higher total calcium balance and bone calcium content just by adding in either sunflower or safflower oil in their diet.

In another study pregnant female rats were made diabetic. They use a chemical called streptozotocin to duplicate the disorder in the animals.  They were then fed evening primrose oil (GLA) at 500 mg/kg/d throughout their pregnancy and found an almost complete restoration of bone ossification (process of laying down new bone) occurred just by adding in the primrose oils (Braddock, Pediatr Res. 2002).

Claassen et al, Prostaglandins 1995, found that the supplementation of essential fatty acids (EFAs) leads to increased intestinal calcium absorption and calcium balance. The main dietary EFAs they used were linoleic acid (LA) from sunflower oil and alpha-linolenic acid (ALA) from flax seed oil.  They were administered in a ratio of 3:1 which is very close to our 4:1 BodyBio Balanced oil.  The calcium balance (mg/24 h) and bone calcium (mg/g bone ash) increased significantly in the group that were on the EFAs as compared to the animals that were not given the oils.

Schlemmer et al, Prostaglandins 1999, found that if you make animal’s essential fatty acid deficient they flat out develop osteoporosis.  He then added in evening primrose oil (GLA) and completely reversed the loss of bone and reported positive effects on bone metabolism in both the growing male and female rat.

It certainly goes against what you might think.  Oils are thin, some of them even squishy, while bone is completely hard as a rock.  But leaning on our visual senses doesn’t work with body chemistry, obviously.

Bone remodeling is a life-long process where mature bone tissue is removed from the skeleton and is called resorption, while new bone tissue is formed.  It’s a process called ossification or new bone formation. These processes go on all the time and are managed by special cells that crawl along our bones and chew up excess bone growth, osteoclast.  There is another cell osteoblast, that busily does the opposite, laying down new growth where it’s needed.

In the first year of life, almost 100% of the skeleton is replaced.  In adults, remodeling proceeds at about 10% per year (Wheeless).  That means that in a span of 10 years our skeleton is brand new,  If the process is continuous those cells that do the work must be directly influenced by essential fatty acids, and if EFAs are needed to get the job done, well…

References

Genuis SJ, Schwalfenberg GK. Picking a bone with contemporary osteoporosis management: Nutrient strategies to enhance skeletal integrity. Clin Nutr. 2007 Apr;26(2):193-207

Haag M, Kearns SD, Magada ON, Mphata PR, Claassen N, Kruger MC. Effect of arachidonic acid on duodenal enterocyte ATPases. Prostaglandins Other Lipid Mediat. 2001 Aug;66(1):53-63

Braddock R, Siman CM, Hamilton K, Garland HO, Sibley CPGamma-linoleic acid and ascorbate improves skeletal ossification in offspring of diabetic rats. Pediatr Res. 2002 May;51(5):647-52.

Claassen N, Coetzer H, Steinmann CM, Kruger MC. The effect of different n-6/n-3 essential fatty acid ratios on calcium balance and bone in rats. Prostaglandins Leukot Essent Fatty Acids. 1995 Jul;53(1):13-9.

Schlemmer CK, Coetzer H, Claassen N, Kruger MC. Oestrogen and essential fatty acid supplementation corrects bone loss due to ovariectomy in the female Sprague Dawley rat. Prostaglandins Leukot Essent Fatty Acids. 1999 Dec;61(6):381-90

Wheeless Textbook of Orthopedics, Clifford R. Wheeless, III, MD.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Aging and The Brain

coconut oil, fats oils, essential fatty acids

Our brains are 60% fat. In light of what we know of brain function and the essential fatty acids that are responsible, the term “fat-head” could now be a complement. Since our brains are in charge and require the right fats to run our thinking machinery, our first priority is to make sure we add the right ones into our diet, the omega 6s and omega 3s. They are essential and get the job done. First – let’s review some of the basics.

Fats and oils can be divided into two densities and two levels. The densities are not unlike the SAE oils, the Society of Automotive Engineers who organize the oils for our autos. But it is better to skip the details at the moment and divide them in two categories “thick” and “thin”. Fats are the thick ones and oils are thin, actually runny. It’s quite good to divide them in this simplistic way. The confusion about what we eventually eat is all over the lot and besides, our cells and membranes organize fats and oils as partners with each having a precise role. The membrane does not work without both, thick and thin, sluggish and active. We can begin with the ones we use in our kitchens because they wind up in our metabolism whether we like it or not.

You can think of the thick ones as butter or lard. We tend to look down on lard as being out of date. We regard it as a thing of the past. Our grandparents and great grandparents certainly didn’t think so. As cooking oil, lard has been with us for some time. It’s been a staple for centuries, probably hundreds of centuries, and we’ve survived and even flourished. It’s part of our evolutionary history. Those thick heavy oils were skimmed off the top of stews and saved, collected from roasts of pork, lamb, goose or turkey. It was regarded as valuable stuff. Before the light bulb, making candles was a basic part of life so the rendering of fat in the kitchen was universal. The plain fact is that lard is OK for cooking. However, just reminiscing, not pushing lard today.

Butter and olive oil are both excellent cooking oils, however, coconut is also marvelous for cooking. It’s not exactly a thick fat, for as you know, it quickly gets thin as the temperature rises. Castillo et al 1999, reports that “Supplementation of coconut oil produced a significant hypercholesterolemia after 7 days of treatment. However, supplementation of menhaden oil induced a significant decrease in total cholesterol after only 2 weeks of treatment”. The raising of cholesterol may sound sacrilegious; however, notwithstanding the loud din of media anti-cholesterol noise, there are those who have difficulty in doing just that – raising cholesterol. Cholesterol is an important fat for our cell membranes; it metabolizes up to our gonadal hormones — think sex. No necessity in elaborating on that subject. It’s also a precursor for our adrenal hormones, which produce our life saving impulses for fight or flight, and bile acids which shepherd the fats and oils around in the blood stream. Without further ado — cholesterol is necessary.

Castillo creates an interesting picture of coconut oil, or butter, as you prefer, and the essential oils that are part of our diet. By itself, coconut can raise cholesterol, but by introducing menhaden oil, it just as quickly reverses and lowers it. This feature of menhaden oil, basically an omega 3 essential fatty acid (EFAs), to lower cholesterol, is also duplicated with the omega 6 EFAs, and there is abundant research that corroborates it. We can regard all of the omega 6s and 3s as “thin oils” and cholesterol, when grouped together as a very “thick fat”.

The lesson here is more than casual. We need the thick ones and we desperately need the thin ones. The thin ones keep the thick ones from collecting to the degree where we tend to get into trouble that comes with aging, such as atherosclerosis, heart disease. In just these two words, thick and thin, we have covered half of all Fatty Acid biochemistry in human metabolism. But it may be just too simple to be looked at with the respect that it deserves. You may spend a third of your life getting a medical degree and half again practicing medicine, but if you do not see this simple relationship you will also retire as a failure from your chosen field of medicine.

Coconut used to be the preferred oil for making popcorn, but ADM and the other large oil producers chased it out of the movies over 30 years ago. It’s a shame we lost it. It was much healthier eating coconut oil than what is currently in use today. Most of the oils used for popcorn and fries are PUFAs, they are thin and should not be heated. They quickly degenerate and become partially hydrogenated and/or oxidize and become rancid.

Coconut oil is one of the most stable oils you can buy. It does not turn rancid easily. It does not attack your arteries. In fact, coconut oil was one of the foods Dr. Weston Price studied when he traveled the world searching for healthier people and their lifestyles. In his journeys he discovered that the coconut was considered a medicine food by the local populations. He found that those civilizations that consumed coconut regularly had no knowledge of cancer, heart disease, arthritis, or diabetes.

There are few other choices for cooking unless you think of the new GMO oils like high oleic soybean, sunflower or safflower oils, Canola also fits into that group because it was one of the first GMO oils to be converted. Canola contains erucic acid, a very long chain saturated fat. It is unhealthy for our membranes, it’s too long and slows the fluidity of the membrane. Think of erucic as a gawking fat blocking our healthy fats from doing what they want to do, running quickly in our membranes managing our cells. Please avoid canola. We simply do not like GMOs for anything we eat.

The thin oils, the PUFAs, come from seeds, nuts, and grains like olive, sunflower, corn, walnut, etc. They harbor the essential fatty acids which play a vital role when the time comes for them to reproduce new versions of themselves. Oils like olive are mostly Mono-Unsaturated Fatty Acids (MUFAs), and are OK, but do not stack up with the likes of the omega 6 and 3 PUFAs, the very healthy FAs. These Poly-Unsaturated Fatty Acids, with more than one double bond, are the stars in our choices of foods. They are predominantly made up of the essential oils, the omega 6s and the omega 3s and are exclusively made by plant seeds. They are important for life and especially the brain. When we use the term essential, we mean that the body cannot function without them. They are essential for life, our life. They hold the secret to Brain health, which we will delve into on Aging and the Brain: Part 2.

To learn more about one of the most important EFA discoveries of the last century, the ratio of 6s and 3s, which is 4: 1, 80% omega 6 (linoleic) to 20% omega 3 (linolenic), go tohttp://www.bodybio.com/BodyBio/docs/BodyBioBulletin-4to1Oil.pdf.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Diabetes and Omega-3’s

Diabetes, Omega-3 fatty acids Super FoodsReading, interpreting and understanding scientific literature can be tedious because the authors often find that their previous paper on the subject missed its mark or was completely wrong. Easy to do when you are blazing new trails; however, the caution they go through to cover their tracks oftentimes makes for difficult reading. Luc Djousse and his colleagues at the U of Washington reported in the May 18, 2011 edition of the American Journal of Clinical Nutrition that, “With the use of objective biomarkers, long-chain omega 3 Fatty Acids (FAs) and Alpha-Linolenic Acid (ALA) were not associated with a higher incidence of diabetes. Individuals with the highest concentrations of both types of FAs had lower risk of diabetes.”

Speed reading is absolutely out of place. Omega-3 fatty acids in the body help to control the inflammation process, which is a benefit because the start of the healing process—initiated by the omega-6 arachidonic acid—also involves the possibility of getting carried away with the exercise. Say you have a cut or abrasion. The key activity that ensues is to stop the loss of fluids – save the blood.  It is that process which tells the body to start the healing by sending white blood cells and platelets to the site of the wound and to agglomerate and close the exit door by swelling the tissues, which is also another way of looking at inflammation. To inflame can be life saving. The omega-3’s are then involved in the work of modulating the activity helping to ease the inflammation that comes with the correction process.

Fatty acids, especially those that are long and highly unsaturated, increase cell membrane fluidity and functionality. Fatty acids are essential to membrane activity at the location of hormone receptors. Insulin resistance in adult-onset diabetes is directly associated with fewer membrane enhancing long-chain fatty acids, largely due to impaired function of desaturase and elongase enzymes needed for a healthy membrane. Ruiz-Gutierrez 1993, “We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids mainly at the expense of docosahexaenoic acid, DHA, and arachidonic acid C20:4n6”.

Cell membrane abnormalities in lipid content are found to be related to poor metabolic control, which is a characteristic of diabetes. Diet is a very important  factor, and interventions with dietary essential fatty acids (EFAs) in the correct ratio (found to be 4:1, omega-6:omega-3), can make a difference. Decsif  T., 2002, “Reduced availability of long-chain polyunsaturates in diabetic children suggests that an enhanced dietary supply of long-chain polyunsaturates may be beneficial”. Children with diabetes demonstrate a deficit of long-chain fatty acids, so incorporating them into a child’s diet is prudent. An unspoken benefit in the application of EFA’s to diabetes treatment is the decrease in triglyceride levels, themselves striking indicators of the potential for cardiovascular issues and very often appearing in persons with diabetes.

Herein resides the prolonged physiological support of the EFAs. For those who lack the efficient conversion of the omega-3 alpha linolenic acid from plant sources (notably flaxseeds and their oil) to EPA and DHA, fish oil may be a viable alternative. In fact the the FA conversion process with diabetes is almost non-existent, but also common with aging.

For quite some time the essential fatty acids have been misunderstood. Of the types of fatty acids, the omega-3’s have received the most publicity, having been applauded for positive health effects, principally, because over the last century the general population ate little fish and had little or no n-3s in the diet. Unless they were more or less health nuts, few did not have any exposure to omega 3s as in flax, and even if they did their ability to elevate up to EPA and DHA was minimal. Fish oil was the answer but the explosion that ensued caused over-consumption and still does.

Hence the comments of Djousse et al that n-3 FAs did not increase diabetes but if both the omega 6s and the 3 s were added together there was marked improvements. There is an inference that n-3s were of no benefit and needed the balance of both EFAs, which we applaud and so should you. Balance is paramount.

References

Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011 May 18.

Ruiz-Gutierrez V, Stiefel P, Villar J, García-Donas MA, Acosta D, Carneado J.  Cell membrane fatty acid composition in type 1 (insulin-dependent) diabetic patients: relationship with sodium transport abnormalities and metabolic control.  Diabetologia. 1993 Sep;36(9):850-6.

T. Decsif, H. Minda, R. Hermann, A. Kozári, É. Erhardt, I. Burus, Sz. Molnár and Gy. Soltész  Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children  Prostaglandins, Leukotrienes and Essential Fatty Acids. 67(4); Oct 2002: 203-210

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Soda and Obesity

type 2 diabetes, obesityWhile a major study relating soda and obesity was done in California, the hypothesis, observations and outcomes are applicable to all the states of the Union.  More than half the adolescents in that state and almost a fourth of the adults treat themselves to at least one sweetened beverage every day.  One of the concerns expressed by UCLA researchers is that the serving size has grown from an average of 6.5 ounces and eighty-eight calories in the 1950’s to 20 ounces and two hundred sixty-six calories by the 2000’s.  In fast food restaurants in 2003, the average serving was 23 ounces (almost 300 calories).  These added caloric sweeteners, including high fructose corn syrup, are not only markers of a poor diet, but also are associated with overweight and obesity in all age groups.

CITATIONS FROM REPORT / ARTICLE
The UCLA Health Policy Research Brief from September, 2009, reports from its data that, “Adults who drink soda occasionally (not every day) are 15% more likely to be overweight or obese, and adults who drink one or more sodas per day are 27% more likely to be overweight or obese than adults who do not drink soda, even when adjusting for poverty status and race/ethnicity.”  Even though the prevalence of overweight in children is lower than in adults, the rates among children have increased more.  In fact, overweight has tripled in teenagers and quadrupled in those from six to eleven years old in the last three decades.  In California the cost of obesity approaches twenty-one billion dollars a year, burdening families, employers and the health care industry.  The study comments that, “California spends more public and private money on the health consequences of obesity than any other state.”  To compound the matter, the article admits that “…drinking soda is also associated with increased risk for type 2 diabetes.”

COMMENTARY
One third of American adults are obese. Their health care costs $1500 more a year than it does for an average-weight person.  The Center for Disease Control announced in July, 2011, that obesity in the entire United States costs $147 billion a year in direct medical costs.  Dr. Thomas R. Frieden, director of the CDC, said the problem is “getting worse rapidly.  The average American is now 23 pounds overweight.”  For Medicare, the cost of obesity is 72% greater just for prescription drugs.  The CDC says that one in three children born in 2000 will develop diabetes.  How did we get there?  Diet.  Does the rest of the world share the problem?  Yes.  Where does the blame go?  White flour, white sugar, high fructose corn syrup, soft drinks and fast food.

Whether it gets marketed as corn sugar or as high fructose corn syrup, which is what it is, this commodity is not equal to other sweeteners when it comes to weight gain.  HFCS costs less than table sugar because, being liquid, it’s easier to transport and blend.  It’s sweeter than sucrose (table sugar), so less is needed, and it’s cheaper because of a combination of corn subsidies and sugar tariffs and quotas.  Cheap corn, in fact, is the building block of the fast-food nation.  Cheap corn created the chubby 20-ounce bottle of soda we have today.

High fructose corn syrup commonly is 55% fructose and 45% glucose, somewhat different from the 50-50 mix in table sugar, where one fructose molecule is attached to one glucose molecule.  Some HFCS may be as high as 80% fructose.  Since all sugars contain four calories per gram, there must be something else about fructose that matters.  Fructose is metabolized more rapidly that glucose, flooding metabolic pathways and increasing triglyceride storage.   It doesn’t spur the production of insulin or leptin, the hormone that sequesters appetite.  The body then lacks satiety.  This elevates serum triglycerides and increases fat storage.  Since it may have less impact on appetite than glucose, fructose contributes to weight gain.  Ingesting lots of fructose may also reduce insulin sensitivity.  (Beck-Nielsen, 1980)

Soft drink consumption has more than doubled in the twenty years from 1977 to 1997.  Not surprisingly, obesity followed the same trend. Cause and effect? It’s been estimated that for each additional sweet drink consumed per day, the odds of obesity increase by sixty percent.  A study of more than fifty thousand nurses by Harvard compared time periods from 1991-1995 and 1995-1999, and found that women whose soda consumption increased had bigger rises in body-mass index than those who drank less or the same amounts of soda. Fast food seems to go well with it.  Unhealthy foods get along nicely with each other.

The debate between the soft drink industry and the health nuts is ongoing.  People who consume lots of fresh-squeezed juices, vegetables and fruits are not the same group that consumes soda and cold cut sandwiches.  The daily calories from soft drinks account for almost a fourth of the recommended daily intake for many Americans, who drink almost fifty-six gallons of soda a year.

In case you’re interested, more than 30% of Americans are obese. More than 24% of Mexicans, 23% of British, 22% of Slovakians, 22% of Greeks and Australians, 21% of New Zealanders, and 15% of Czechs, but only 3% of Japanese and Koreans. Go figure. Obesity, by the way, means being more than 20% above ideal weight for height.

References

UCLA Health Policy Research Brief
September 2009
Bubbling Over: Soda Consumption and Its Link to Obesity in California
Susan H. Babey, Malia Jones, Hongjian Yu and Harold Goldstein

In California, 62% of adolescents ages 12-17 and 41% of children ages 2-11 drink at least
one soda or other sweetened beverage every day. In addition, 24% of adults drink at least
one soda or other sweetened beverage on an average day. Adults who drink soda occasionally
(not every day) are 15% more likely to be overweight or obese, and adults who drink one or
more sodas per day are 27% more likely to be overweight or obese than adults who do not
drink soda, even when adjusting for poverty status and race/ethnicity.

The prevalence of overweight and obesity has increased dramatically in both adults
and children in the last three decades in the United States. In the 1970s, about 15% of
adults were obese and by 2004 the rate had climbed to 32%.1 Although the prevalence of
overweight among children is lower than among adults, the rates among children and
adolescents have increased considerably more. The prevalence of overweight and obesity
nearly tripled among 12-19 year olds and more than quadrupled among 6-11 year olds
in the last three decades.

In California, 21% of adults are currently obese and an additional 35% are overweight. Among adolescents, 14% are obese and another 16% are overweight.2 Similar to national trends, the trend in California is toward increasing weight in both adults and adolescents.3 Each year in California, overweight and obesity cost families, employers, the health care industry and the government $21 billion.4 California spends more public and private money on the health consequences of obesity than any other state.5

Overweight and obesity are associated with serious health risks. In children and adolescents, overweight and obesity are associated with increased risk for cardiovascular disease indicators including high total cholesterol, high blood pressure, and high fasting insulin, an early indicator of diabetes risk.6 In addition, overweight children and adolescents are more likely to be overweight or obese as adults.7 In adults, overweight and obesity are associated with increased risk for diabetes, heart disease, stroke, some types of cancer and premature death.1, 8, 9

Drinking sweetened beverages such as soda and fruit drinks that have added caloric sweeteners (e.g., sucrose, high fructose corn syrup) is one marker of a poor diet, and is
associated with overweight and obesity in people of all ages.10-13 A number of studies have found that greater consumption of sweetened beverages is associated with overweight and obesity among both adults and children.12-19 In addition, randomized controlled trials that examine the impact of reducing intake of sweetened beverages on weight indicate
that reducing consumption of soda and other sweetened drinks leads to reductions in
overweight and obesity.20, 21 Among adults, drinking soda is also associated with increased risk for type 2 diabetes.13 Moreover, drinking sweetened beverages has
increased, and it is now more common than ever, particularly among adolescents.22
Between 1977 and 2002 Americans increased their calorie intake from soft drinks by
228%.23 Portion sizes have also increased from an average serving size of 6.5 fl oz (88 calories) in the 1950s, to 12 fl oz (150 calories), 20 fl oz (266 calories), and even larger portion sizes common today.24-26 The average serving size of soft drinks in fast food restaurants in 2002 was 23 fl oz (299 calories), with some chains now commonly selling soft drinks in 32 to 64 fl oz portions (416 to 832 calories, respectively).27 Sweetened beverages are a significant contributor to total caloric intake, especially for children and adolescents, and they lack the nutrients our bodies need.24, 26, 28

Additionally, eating habits established in childhood are important determinants of
eating habits as adults.29, 30
http://www.healthpolicy.ucla.edu/pubs/files/Soda%20PB%20FINAL%203-23-09.pdf

SUPPORTING ABSTRACTS
Am J Clin Nutr February 1980 vol. 33 no. 2 273-278
Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects
H Beck-Nielsen, O Pedersen and HO Lindskov

We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety. Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day. The dietary regimens continued for 1 week. Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose, insulin, and ketone bodies in the two groups studied. High- glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding (P less than 0.05) and insulin sensitivity (P less than 0.05). The changes in insulin binding and insulin sensitivity correlated linearly (r = 0.52, P less than 0.01). We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose.

Medscape J Med. 2008;10(8):189. Epub 2008 Aug 12.
Soft drinks and weight gain: how strong is the link?
Wolff E, Dansinger ML.
Boston University School of Medicine, Boston, Massachusetts, USA. [email protected]

CONTEXT
Soft drink consumption in the United States has tripled in recent decades, paralleling the dramatic increases in obesity prevalence. The purpose of this clinical review is to evaluate the extent to which current scientific evidence supports a causal link between sugar-sweetened soft drink consumption and weight gain.

EVIDENCE ACQUISITION
MEDLINE search of articles published in all languages between 1966 and December 2006 containing key words or medical subheadings, such as “soft drinks” and “weight.” Additional articles were obtained by reviewing references of retrieved articles, including a recent systematic review. All reports with cross-sectional, prospective cohort, or clinical trial data in humans were considered.

EVIDENCE SYNTHESIS
Six of 15 cross-sectional and 6 of 10 prospective cohort studies identified statistically significant associations between soft drink consumption and increased body weight. There were 5 clinical trials; the two that involved adolescents indicated that efforts to reduce sugar-sweetened soft drinks slowed weight gain. In adults, 3 small experimental studies suggested that consumption of sugar-sweetened soft drinks caused weight gain; however, no trial in adults was longer than 10 weeks or included more than 41 participants. No trial reported the effects on lipids.

CONCLUSIONS
Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.  PMID: 18924641

Diabetes Care. 2010 Nov;33(11):2477-83. Epub 2010 Aug 6.
Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis.
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB.

Department of Nutrition, Harvard School of Public Health, and Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA.

OBJECTIVE
Consumption of sugar-sweetened beverages (SSBs), which include soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks has risen across the globe. Regular consumption of SSBs has been associated with weight gain and risk of overweight and obesity, but the role of SSBs in the development of related chronic metabolic diseases, such as metabolic syndrome and type 2 diabetes, has not been quantitatively reviewed.

RESEARCH DESIGN AND METHODS
We searched the MEDLINE database up to May 2010 for prospective cohort studies of SSB intake and risk of metabolic syndrome and type 2 diabetes. We identified 11 studies (three for metabolic syndrome and eight for type 2 diabetes) for inclusion in a random-effects meta-analysis comparing SSB intake in the highest to lowest quantiles in relation to risk of metabolic syndrome and type 2 diabetes.

RESULTS
Based on data from these studies, including 310,819 participants and 15,043 cases of type 2 diabetes, individuals in the highest quantile of SSB intake (most often 1-2 servings/day) had a 26% greater risk of developing type 2 diabetes than those in the lowest quantile (none or <1 serving/month) (relative risk [RR] 1.26 [95% CI 1.12-1.41]). Among studies evaluating metabolic syndrome, including 19,431 participants and 5,803 cases, the pooled RR was 1.20 [1.02-1.42].

CONCLUSIONS
In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases.

J Public Health Policy. 2004;25(3-4):353-66.
The obesity epidemic in the United States.
Morrill AC, Chinn CD.
Capacities Inc., Watertown, Massachusetts 02471, USA. [email protected]

We describe the epidemic of obesity in the United States: escalating rates of obesity in both adults and children, and why these qualify as an epidemic; disparities in overweight and obesity by race/ethnicity and sex, and the staggering health and economic consequences of obesity. Physical activity contributes to the epidemic as explained by new patterns of physical activity in adults and children. Changing patterns of food consumption, such as rising carbohydrate intake–particularly in the form of soda and other foods containing high fructose corn syrup–also contribute to obesity. We present as a central concept, the food environment–the contexts within which food choices are made–and its contribution to food consumption: the abundance and ubiquity of certain types of foods over others; limited food choices available in certain settings, such as schools; the market economy of the United States that exposes individuals to many marketing/advertising strategies. Advertising tailored to children plays an important role.  PMID: 15683071

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Indoor Air Pollution

indoor air pollutionIndoor air pollution is one of the most overlooked threats to human health. Households in developing countries might be the hardest hit. Because children spend almost eighty percent of their time indoors, they are the most likely victims. In the past several years it has been determined that conditions ranging from asthma, headaches and fatigue to allergic reactions, hormone imbalances and central nervous damage may be attributed to indoor air quality—or, rather, the lack of it. Most of us realize that outdoor air quality can affect health, but few pay attention to the indoor air…unless it smells bad.

In a paper supported by the University of Medicine and Dentistry of New Jersey and printed in the British Medical Bulletin in the early 2000’s, Junfeng (Jim) Zhang and Kirk Smith allowed that the ubiquitous character of indoor air pollution “…may contribute to increasing prevalence of asthma, autism, childhood cancer, medically unexplained symptoms, and perhaps other illnesses.”   Because the sources of indoor pollution are not expected to abate in the near future, particularly those associated with tobacco use, we can expect to voice concerns for a long time. The authors add that “…risks associated with solid fuel combustion coincide with risk associated with modern buildings.”

COMMENTARY
It is absurd that indoor air quality should be so poor that it causes sickness and disease, yet that appears to be more the rule than the exception in modern times.  Nobody would think of running a tractor-trailer or a tour bus in the living room, but the pollution effect is the same.  Most of us are unaware of the problem because a single major source of indoor pollution can’t be fingered. Despite this unrecognized threat, indoor pollution is twice as bad as outdoor, according to studies performed by the Bloomberg School of Public Health at Johns Hopkins.  Others put the rate at five times. There are so many sources of indoor pollution that have become part of our daily lives that we never question them. Have you thought about the unpronounceable ingredients in your cleaning products and other household chemicals, like the pesticides you use in the yard? How about your cosmetics and the smelly things you plug into the wall to hide other smelly things?  Got new carpet or upholstery? Oh, yeah, there are more, such as the aroma of hot tar being applied to the new roof at your children’s school…while school’s in session. The activity may be outdoors, but the sickening smell is certainly indoors.

The influx of biological pollutants is hard to manage.  Molds, bacteria, viruses, animal dander, skin particles (yes, even human), pollen and dust mites are everywhere.  You can see airborne particles in that beam of sunshine coming through the window, but you can’t identify any of them.  Some can breed in the stagnant water that sits in your humidifier, or where water has collected in your ceiling tiles, insulation or carpet.  These things can cause fever, chills, cough, and chest tightness, among other symptoms.  Even when we do what we think is good for the family, we may do the opposite.  Burning the woodstove or fireplace might save money on the heating bill (though the fireplace is suspect), but how about the junk it puts into the air?  You can’t win, eh?

In our attempts to conserve energy, we have sealed our houses so tightly that nothing can get in and less can get out.  Once we change the air pressure dynamics of our houses, we have allowed intruders to enter.  Radon and soil gases are most common, and they creep through the cellar floor.  Mechanical ventilation can help to get the junk out and bring at least some fresher air in.  Not only does insulation contribute to the tightness of our homes, but also it brings problems of its own in the form of irritating chemicals.

Increasing ventilation is one of the easiest steps to improving indoor air quality.  Even in the dead of winter it’s a good idea to open the front and back doors simultaneously once a day to let fresh cold air in and the stale reheated air out.  Pathogens grow in an environment that is warm, dark and damp.  Your hot-air heater is a prime breeding ground for colds and the like.  The American Lung Association and the Mayo Clinic have recognized air filters as being sufficiently effective to allay at least some of the problem.   Using a vacuum with a HEPA filter is another prudent intervention.

Concerning household cleaners, we all know that anything natural costs more than anything man-made, and that mindset is hard to figure out.  Why do we have to pay for things that are left out?  In the mean time, note that vinegar-water concoctions are just as good as many commercial products at cleaning our homes—even the commode.  Who cares if it smells like salad?

But what might just be the best air cleaner on the planet is a collection of house plants.  Formaldehyde is a major contaminant of indoor air, originating from particle board, carpets, window coverings, paper products, tobacco smoke, and other sources.  These can contribute to what has been called “sick building syndrome.”  The use of green plants to clean indoor air has been known for years.  This phytoremediation has been studied with great intensity in a few laboratories across the globe, where it was learned that ferns have the greatest capability of absorbing toxins.  (Kim, Kays. 2010)  As is the case with many endeavors, there is a hierarchy of plants that does the job.  After the ferns, the common spider plant (Chlorophytum comosum) was found best at removing gaseous pollutants, including formaldehyde.  Way back in 1984 NASA released information about how good the spider plant is at swallowing up indoor air pollution.  The heartleaf philodendron partners well with Chlorophytum.  Dr. Bill Wolverton, retired from NASA, has a list (http://www.sti.nasa.gov/tto/Spinoff2007/ps_3.html).  Areca and lady palms, Boston fern, golden pothos and the dracaenas are at the top.  Plants with fuzzy leaves are best at removing particulates from smoke and grease, and some are even maintenance-free (almost), including the aloes, cacti, and the aforementioned spider plants, pothos and dracaenas, the last sometimes called the corn plant.

For more information, try these resources:

Indoor Air Pollution Increases Asthma Symptoms (Johns Hopkins Bloomberg School of Public Health)
http://www.jhsph.edu/publichealthnews/press_releases/2009/breysse_indoor_asthma.html

Pollution at Home Often Lurks Unrecognized (12/26/2008, Reuters Health) by Amy Norton
http://www.reuters.com/article/2008/12/26/us-pollution-home-idUSTRE4BP1ZL20081226

Air Purifiers and Air Filters Can Help the Health of Allergy and Asthmas Sufferers (S. A. Smith)
http://ambafrance-do.org/alternative/11888.php

Indoor Air Pollution Fact Sheet (08/1999, American Lung Association)
http://www.lungusa.org/healthy-air/home/healthy-air-at-home/

An Introduction to Indoor Air Quality (Environmental Protection Agency)
http://www.epa.gov/iaq/ia-intro.html

References

Br Med Bull (2003) 68 (1): 209-225.
Indoor air pollution: a global health concern
Junfeng (Jim) Zhang and Kirk R Smith

Environmental and Occupational Health Sciences Institute & School of Public Health, University of Medicine and Dentistry of New Jersey, NJ

Indoor air pollution is ubiquitous, and takes many forms, ranging from smoke emitted from solid fuel combustion, especially in households in developing countries, to complex mixtures of volatile and semi-volatile organic compounds present in modern buildings. This paper reviews sources of, and health risks associated with, various indoor chemical pollutants, from a historical and global perspective. Health effects are presented for individual compounds or pollutant mixtures based on real-world exposure situations. Health risks from indoor air pollution are likely to be greatest in cities in developing countries, especially where risks associated with solid fuel combustion coincide with risk associated with modern buildings. Everyday exposure to multiple chemicals, most of which are present indoors, may contribute to increasing prevalence of asthma, autism, childhood cancer, medically unexplained symptoms, and perhaps other illnesses. Given that tobacco consumption and synthetic chemical usage will not be declining at least in the near future, concerns about indoor air pollution may be expected to remain.

SUPPORTING ABSTRACTS
Nippon Eiseigaku Zasshi. 2009 May;64(3):683-8.
[Indoor air pollution of volatile organic compounds: indoor/outdoor concentrations, sources and exposures]. [Article in Japanese]
Chikara H, Iwamoto S, Yoshimura T.
Fukuoka Institute of Health and Environmental Sciences, Mukaizano, Dazaifu, Fukuoka 818-0135, Japan. [email protected]

In this review, we discussed about volatile organic compounds (VOC) concentrations, sources of VOC, exposures, and effects of VOC in indoor air on health in Japan. Because the ratios of indoor concentration (I) to outdoor concentration (O) (I/O ratios) were larger than 1 for nearly all compounds, it is clear that indoor contaminations occur in Japan. However, the concentrations of basic compounds such as formaldehyde and toluene were decreased by regulation of guideline indoor values. Moreover, when the sources of indoor contaminations were investigated, we found that the sources were strongly affected by to outdoor air pollutions such as automobile exhaust gas. Since people live different lifestyles, individual exposures have been investigated in several studies. Individual exposures strongly depended on indoor concentrations in houses. However, outdoor air pollution cannot be disregarded as the sources of VOC. As an example of the effect of VOC on health, it has been indicated that there is a possibility of exceeding a permissible cancer risk level owing to exposure to VOC over a lifetime.

Environ Sci Technol. 2009 Nov 1;43(21):8338-43.
Uptake of aldehydes and ketones at typical indoor concentrations by houseplants.
Tani A, Hewitt CN.
Institute for Environmental Sciences, University of Shizuoka, Shizuoka 422-8526, Japan. [email protected]

The uptake rates of low-molecular weight aldehydes and ketones by peace lily (Spathiphyllum clevelandii) and golden pothos (Epipremnum aureum) leaves at typical indoor ambient concentrations (10(1)-10(2) ppbv) were determined. The C3-C6 aldehydes and C4-C6 ketones were taken up by the plant leaves, but the C3 ketone acetone was not. The uptake rate normalized to the ambient concentration C(a) ranged from 7 to 19 mmol m(-2) s(-1) and from 2 to 7 mmol m(-2) s(-1) for the aldehydes and ketones, respectively. Longer-term fumigation results revealed that the total uptake amounts were 30-100 times as much as the amounts dissolved in the leaf, suggesting that volatile organic carbons are metabolized in the leaf and/or translocated through the petiole. The ratio of the intercellular concentration to the external (ambient) concentration (C(i)/C(a)) was significantly lower for most aldehydes than for most ketones. In particular, a linear unsaturated aldehyde, crotonaldehyde, had a C(i)/C(a) ratio of approximately 0, probably because of its highest solubility in water.

Proc Am Thorac Soc. 2010 May;7(2):102-6.
Indoor air pollution and asthma in children.
Breysse PN, Diette GB, Matsui EC, Butz AM, Hansel NN, McCormack MC.
Department of Environmental Heath Sciences, Johns Hopkins University Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD 21205, USA. [email protected]

The purpose of this article is to review indoor air pollution factors that can modify asthma severity, particularly in inner-city environments. While there is a large literature linking ambient air pollution and asthma morbidity, less is known about the impact of indoor air pollution on asthma. Concentrating on the indoor environments is particularly important for children, since they can spend as much as 90% of their time indoors. This review focuses on studies conducted by the Johns Hopkins Center for Childhood Asthma in the Urban Environment as well as other relevant epidemiologic studies. Analysis of exposure outcome relationships in the published literature demonstrates the importance of evaluating indoor home environmental air pollution sources as risk factors for asthma morbidity. Important indoor air pollution determinants of asthma morbidity in urban environments include particulate matter (particularly the coarse fraction), nitrogen dioxide, and airborne mouse allergen exposure. Avoidance of harmful environmental exposures is a key component of national and international guideline recommendations for management of asthma. This literature suggests that modifying the indoor environment to reduce particulate matter, NO(2), and mouse allergen may be an important asthma management strategy. More research documenting effectiveness of interventions to reduce those exposures and improve asthma outcomes is needed.

HortScience 45: 1489-1495 (2010)
Variation in Formaldehyde Removal Efficiency among Indoor Plant Species
Kwang Jin Kim1, Myeong Il Jeong, Dong Woo Lee, Jeong Seob Song, Hyoung Deug Kim, Eun Ha Yoo, Sun Jin Jeong and Seung Won Han

The efficiency of volatile formaldehyde removal was assessed in 86 species of plants representing five general classes (ferns, woody foliage plants, herbaceous foliage plants, Korean native plants, and herbs). Phytoremediation potential was assessed by exposing the plants to gaseous formaldehyde (2.0 µL·L–1) in airtight chambers (1.0 m3) constructed of inert materials and measuring the rate of removal. Osmunda japonica, Selaginella tamariscina, Davallia mariesii, Polypodium formosanum, Psidium guajava, Lavandula spp., Pteris dispar, Pteris multifida, and Pelargonium spp. were the most effective species tested, removing more than 1.87 µg·m–3·cm–2 over 5 h. Ferns had the highest formaldehyde removal efficiency of the classes of plants tested with O. japonica the most effective of the 86 species (i.e., 6.64 µg·m–3·cm–2 leaf area over 5 h). The most effective species in individual classes were: ferns—Osmunda japonica, Selaginella tamariscina, and Davallia mariesii; woody foliage plants—Psidium guajava, Rhapis excels, and Zamia pumila; herbaceous foliage plants—Chlorophytum bichetii, Dieffenbachia ‘Marianne’, Tillandsia cyanea, and Anthurium andraeanum; Korean native plants—Nandina domestica; and herbs—Lavandula spp., Pelargonium spp., and Rosmarinus officinalis. The species were separated into three general groups based on their formaldehyde removal efficiency: excellent (greater than 1.2 µg·m–3 formaldehyde per cm2 of leaf area over 5 h), intermediate (1.2 or less to 0.6), and poor (less than 0.6). Species classified as excellent are considered viable phytoremediation candidates for homes and offices where volatile formaldehyde is a concern.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Importance of Iodine

Importance of IodineIodine (I) is essential, which clearly means we need it. Just as we need zinc or magnesium, we need I. The common iodine deficiency disorders include goiter, hypothyroidism, mental retardation, reproductive impairment, and decreased child survival; however that short group is only the beginning of health problems with a lack of iodine. The recent meltdown of the nuclear power stations in Japan may have highlighted the urgent need for Iodine, but even though the threat has passed, the health requirement for I has not diminished. It’s even more important than we have been led to believe.

David Derry MD PhD, “Fibrocystic disease of the breast consists of small or large, sometimes painful lumps in women’s breasts. It varies in the way it shows—not only in different women, but also because it changes from month to month in the same women. Medical doctors generally believe that fibrocystic disease results from the excess number of cells that grow in the breast during the menstrual cycle from the hormonal stimulation.

“Since the number of cells increases in the breast during the cycle, some of the cells have to be removed to restore the normal condition each month. Iodine is the trigger mechanism that causes excess cells to disappear to complete this normal process of cell death. Without enough iodine, the extra cells that develop during the menstrual cycle due to the hormonal stimulation do not resolve back to the normal breast architecture. These leftover cells build up over repeated cycles and cause the lumps, soreness, and larger lesions of fibrocystic disease.

“However, while about 90 percent of North American women have fibrocystic disease, about 40 percent of these women experience no symptoms. Their breasts may be normal to examination, but at that point the disease may be only microscopically detectable with a biopsy.

“Enough iodine enables the excess cells to be cleared out, and the breast to return to its normal resting state; the fibrocystic disease has slowly disappeared from the breast.

Nobel Laureate Albert Szent Györgyi, the physician who discovered Vitamin C in 1928, commented: “When I was a medical student, iodine in the form of KI (potassium iodide) was the universal medicine. Nobody knew what it did, but it did something and did something good. We students used to sum up the situation in this little rhyme:

If ye don’t know where, what, and why
prescribe ye then K and I”.

“Iodine remains the perfect antiseptic with the least side effects of all time. As a perfect antiseptic killing all single-celled organisms, there has to be a common mechanism of a single element like iodine.

“This is part of a general thesis that both iodine and thyroid hormone act as a team to provide a constant surveillance against abnormal cell development, including carcinogenic chemicals that can spread cancer cells within the body.

“Iodine appears to have several more roles in the body. Iodine protects against abnormal growth of bacteria in the stomach (helicobacter pylori is the most clinically significant). Iodine can coat incoming allergic proteins to make them non-allergic; It also deactivates all biological and most chemical poisons in the stomach.

“”I propose that…iodine and thyroid hormones act as a team to provide a constant surveillance against abnormal cell development and the spread of cancer cells within the body including chemicals that are carcinogenic” writes Dr. Derry, who, in addition to holding an MD, also has a PhD in neurochemistry and is a former University of Toronto Medical Research Council Scholar.  “Cancer grows so slowly when using iodine and thyroid hormone therapy that the cancer will not affect the lives of the patients who have it. The treatment is non-invasive, inexpensive and safe.”

Dr.  Derry also credits iodine with several other roles in the body: It protects against abnormal growth of bacteria in the stomach.  It detoxifies chemicals, food poisoning, snake venom, etc. It coats incoming allergic proteins to make them non-allergic, and probably defuses autoimmune disease mechanisms in the same way.

How much iodine is enough? It has been shown that daily doses of iodine above two to three milligrams per day (about half a drop of Lugols from a standard eyedropper) saturate the thyroid within a couple of weeks. At this point, the thyroid gland stops taking up iodine. This means that at a dietary intake above two to three milligrams, all of the iodine goes to all its other functions in the body, such as killing off abnormal cells.

BodyBio has been marketing Iodine for ~10 years, but after extensive testing has added a Liquid Iodine Taste Testing Kit to its famous Liquid Mineral line. This is the absolute best way to take Iodine safely (or any essential mineral) — taste it first. Use your own taste buds to see if you even need it to begin with. We do that for all the trace minerals (which we desperately need) and guess what – Iodine, if anything, is another essential mineral. There’s no reason that we should not rely on our sense of taste for Iodine just as we have for them all.

Dr Derry suggests about half a drop of Lugols solution. That’s equivalent to ~36 drops of BodyBio Iodine (~2.4 mgs of potassium iodide), very close to a ½ drop of Lugol’s. Why reinvent the wheel, follow the expert’s advice as suggested in Dr. Derry’s book; available on Amazon “Breast Cancer and Iodine: How to Prevent and How to Survive Breast Cancer”.

BOOK-BreastCancer-IodinewebAny good Iodine supplement such as  Lugols®, Iodoral®, or BodyBio Iodine # 9, will suffice. However, BodyBio alone guides you to recognize when you have filled up your Iodine stores, when you have enough. Simply by putting 36 drops of BodyBio Iodine in 8 ounces of filtered water you have created your personal testing solution. Just a taste of the solution is enough to guide you. If it has a pleasant taste (hmm good), or, if there is no taste (plain water) – you need it. If the taste is strong or disturbing – do not take it. It does not get any simpler.  http://www.bodybio.com/BodyBio/docs/BodyBioBulletin-LiquidMinerals.pdf.

You can now fill up your Iodine bucket (or any of the essential minerals that we require). If it’s low (most everyone will be), take 36 drops per day and add that into your daily mineral drink. Please check your taste response often, at least weekly, to avoid taking an excess of I or any mineral you do not need. This is too important to put off. Call BodyBio at 888 320 8338 and order the New BodyBio Iodine Test Kit – do it today.   

iodine-samples

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.