Category: Uncategorized

The nutritional biology of human skin color


The amount of melanin found within our skin has long been a source of division for humans culturally, but anthropologist Nina Jablonski of Penn State tells the story of how human skin color unites us all biologically.

It’s become one of my favorite stories to share as it relates to nutritional biology: More pigment was naturally selected because it acted as a sunscreen needed to protect against DNA damage and destruction of folate, needed for reproduction. Depigmentation was selected for when humans dispersed from Africa and into the Northern Hemisphere where they needed skin light enough to absorb sufficient UVB rays to produce vitamin D.

I first heard Jablonski discuss the nature of human skin pigmentation almost two years ago at the AAAS conference in Washington DC. Later, I discovered her TED talk, which I’ve posted above. It’s older, but worth watching over and over again. Jablonski has a simple message: instead of using skin color to discriminate, use skin color to teach people about evolution and health.

Now Jablonski has a new, richly illustrated book out called Living Color. It serves to complement to her previous book, Skin Color: A Natural History. You can read an excerpt from her book here, which includes this paragraph:

The properties of our skin — including color — affect our health. Most of us think that humans have used our collective intelligence to overcome biological limitations in a way that cultureless species cannot do. But at least with respect to our skin, this hubris is unwarranted. Many common health problems like skin cancer and vitamin D deficiency are caused by a mismatch between our habits and our heritage. The amount of pigment that our skin contains, which determines how our bodies deal with sunshine, evolved in our ancestors. Today, many of us live under very different conditions from those experienced by our predecessors and pursue dramatically different lifestyles. People living thousands of years ago did not have indoor jobs and go on vacation; they lived outside most of the time and generally didn’t travel much or very far. Because of these factors, many of us have an inherited skin tone that is not adapted to our current circumstances, and that mismatch places us at risk for specific health problems. Knowing our own particular risk factors can be a matter of life or death.

What journalists should know before writing about fructophobia

In his new book, Fat Chance, Dr. Robert Lustig argues that “sugar is more toxin than it ever was nutrient.” He writes that sugar is as addictive as cocaine, that it should be regulated like tobacco, and that children should be carded before having a soda. He compares the fructose component of sugar to ethanol. “Pick your poison,” he writes, arguing that fructose will “fry your liver and cause all the same diseases as does alcohol.” He also challenges energy balance (calories-in-calories-out) as the dominant paradigm of understanding obesity and and argues that sugar is harmful in ways beyond the calories it provides.

With statements as controversial as these, it’s no wonder that the media, who tend to crave sensationalism to obtain readers or viewers, eat them up like candy. And Dr. Lustig knows what he’s doing and just what to say to elicit attention. He’s no stranger to the spotlight, as Elizabeth Weil writes in her article featuring the pediatric endocrinologist. The showman-doctor also knows just how to tell a classic falling-prey-to-cruelty story. He’d have his readers believe just what they want to hear: that their weight gain is not their fault, that the great evil monster of the food industry is putting addictive “poison” in their food in the form of sugar, and that the government is standing “idly by” letting it all happen. After reading Dr. Lustig’s book, it’s easy to understand why readers are entertained and maybe even enraged enough to give up on sugary sodas, cheese cake, and apple pie. But are the arguments Dr. Lustig makes in the book right or wrong?

Sparked by my ire of journalists buying into the sensationalism without so much as offering a contrasting view, I previously wrote about how Dr. Lustig’s eyebrow-raising claims didn’t appear to hold water. For example, one need only check the evidence from systematic reviews of human intervention trials (not rodents) to find that: 1) fructose has no significant effects on body weight, blood pressure, or uric acid when compared to other carbohydrates contributing the same amount of calories in the diet; 2) fructose in high doses providing excess calories increases body weight as expected from its contribution of excess calories and not because of any unique property of fructose; 3) and fructose at the levels normally found in fruit, which equals to around 10 grams per meal, is shown to improve glycemic control long-term. Does that sound like an ingredient that is “toxic”? I didn’t think so and neither do most nutrition scientists who’ve reviewed the evidence. For these reasons, scientists lashed out against Dr. Lustig’s inflammatory rhetoric and overstatements in a symposium sponsored by the Corn Refiner’s Association at Experimental Biology last April. I wrote about the debate, which I dubbed the “Sugar Showdown“, and then followed up with an interview with Dr. John Sievenpiper, a lead author of several systematic reviews and meta-analyses evaluating fructose’s effects on health of the body, to bring more clarity to the subject.

Despite the push-back from his scientist-peers, however, it’s evident that Dr. Lustig is pressing on with his mission to demonize sugar and his published book has gained him plenty of new attention in articles and interviews. I’ve found it difficult to keep up with it all and have lagged behind, having been busy with other projects (like moving to a new house). Fortunately, exercise physiologist and sports dietitian David Driscoll took up the charge to set the record straight on fructose around the World Wide Web. I’m indebted to Driscoll for nicely summarizing my own thoughts, pushing my blog article, and bringing my attention to other articles. And I would encourage any journalist or blogger who is writing about sugar, fructose, or Dr. Lustig’s book first read Driscoll’s comment and follow each of the links. He told me over Twitter that he posted the following comment, or ones like it, on at least 50 different sites over five days:

While Dr Lustig’s theories and evidence may seem convincing to the general public and reporters, the real test is how well he performs with his fellow scientists!
He was certainly called out for overstating the evidence and poorly extrapolating rat research at a conference he spoke at earlier in the year – check out the Q and A video in the attached article by David Despain (as well as the other lectures)!
What research shows that it is fructose that causes addiction? At the Q and A at the Sugar Symposium, Dr Lustig was called out on this and one researcher showed that rats liked glucose based carbohydrates over sucrose, and another questioned the applicability of rat research to be extrapolated to humans!
Also a recent rat studied suggests that it might be the sweet taste and NOT the fructose (as they used an artificial sweetener) although the article title gets it wrong also!
http://www.health.msn.co.nz/healthnews/8582942/sugar-as-addictive-as-coc…
The major issue with Dr Lustig’s theory is looking at US Sugar intake over history – levels were still high in the early 20th century – so saying it is sugar is either an oversimplification or there is a threshold value that we have recently crossed. Methinks that it is a perfect storm of more sugar and less burning it up with physical activity!
I hope you get a chance to review these before the interview – especially the video lectures linked to within the article by David Despain

In my own reading of Dr. Lustig’s book over the last few days, I’ve found that apart from the claims about sugar, the rest of the book is relatively tame. In fact, it reminds me of why I tend to hate popular diet books and find them boring. There is one chapter where Dr. Lustig calls out out insulin as “the bad guy,” as Gary Taubes does, and I’ve discussed why this is shortsighted in my post “Good insulin, bad insulin: Its role in obesity“. He also dismisses physical activity as having a participating role in weight management (although he does say it’s good for you for other reasons); as I’ve written before, exercise is critical because of the role of skeletal muscle in consuming energy and determining metabolic rate. Mainly, however, the book regurgitates a lot of the same arguments about what’s wrong with the food system, some controversial and some not.

Overall, many nutritionists would probably agree that Dr. Lustig’s recommendation are somewhat controversial. He summarizes them by shortening Michael Pollan’s “Eat food. Not too much. Mostly plants.” to just simply “Eat food.” He argues that if you cut out all processed foods and sugar, people are bound to lose weight. He calls for completely cutting out anything with a Nutrition Facts label, which denotes that it is a “processed food”. It’s a no-brainer that people who go to this extreme would likely lose weight from lack of contributing calories from those foods. But it’s not the only approach one can take to lose weight. To say that one can’t include processed foods (even those with fructose) in one’s diet and still be healthy is just a fallacy. There are many people who include processed foods in their diet in moderation and have no problems maintaining their weight. There are also several degrees of processing and several different types of processed foods that make Dr. Lustig’s sweeping statements misleading. In some cases, processed foods (e.g. meal replacements) can be helpful in promoting weight loss.

One might ask, why all the fuss about scientific accuracy? What’s the problem with the cause of getting people to limit intake of sugar if it leads to a common good of reducing obesity? My answer to people who ask me this is the same that other scientists have voiced, which is that singling out of any ingredient and to make it the scapegoat for the obesity epidemic is just distracting. It’s not helpful to call sugar or fructose alone as “toxic” and ultimately does nothing to change people’s habits, except maybe causing them to forgo buying any food with high-fructose corn syrup for a while. In the end, people will still continue to eat too much, exercise too little, and gain weight.

Update 5-13-13: San Diego State University professor Mark Kern, Ph.D., offers a much more thorough scientific review of Dr. Lustig’s book than I ever could. I’d encourage all to read it here (ht Colby Vorland) on the CRA’s “Sweetener Studies” website (no, I have no financial relationship with CRA). From Kern’s review, here are a couple of quotes that best sum up my own thinking:

  • “Dr. Lustig misinterprets the available scientific evidence by making sweeping conclusions based on studies that do not examine real-life consumption patterns.”
  • “The addition of the Nutrition Facts Panel to packaged food was a major step forward in public nutrition education and transparency on behalf of food manufacturers.”
  • “…inaccuracies suggest that the author is not well-versed in the sciences of foods and nutrition or is misleading readers in a way to promote their agreement with his views.”

Of bunnies and bacteria

Rabbit

I remember when I first learned that a rabbit ate its food twice.

This curious dietary practice, called coprophagy, is something I’d witnessed as a child raising my own rabbits and guinea pigs in the backyard. Disgusted by the sight of my pets eating their own feces, I recall trying to keep their cages as clean as possible. Had I known better, I would not have been so quick to remove droppings from their cage because I might’ve put these animals at risk for nutritional deficiency (1-2). Luckily, I wasn’t ever very consistent at keeping their cages clean all the time.

Rabbits and guinea pigs, as it turns out, need to eat their own droppings because they provide a valuable source of nutrients like vitamin B12. In the wild, they will normally leave soft droppings at the mouths of their burrows while they go off foraging at dawn or dusk. When they’ve had their fill of foliage, they return and — far from being repulsed by having a stack of droppings at the foot of their doorstep — they eat up these droppings, which are by this time a nutrient-rich fermented dessert.

Being non-ruminant herbivores, rabbits and guinea pigs are adapted to half-digest their food to re-consume it later. Cows, on the other hand, have millions of microorganisms residing within their own multi-compartmental stomachs working to break down their food and producing nutrients. Other mammals, including sheep, apes, and humans have large intestines where microbes live and flourish. Predators don’t have a need for such large guts, since they can obtain their nutritional requirements from prey.

Interestingly, humans share a behavior with rabbits and guinea pigs: not that we eat our own feces, but that we allow food to ferment for full nourishment later. Although humans are unique in the sense that we’ve developed quite a taste for fermented foods. The sheer variety we eat is mesmerizing: yogurt, cheese, wine, beer, vinegar, pickles, kefir, olives, breads, miso and kimchi. All human cultures are dependent on fermented products of some kind as a food source leading to a large variety of human microbiotas across the world (3, 4). Fermented foods are deeply interwoven into the human tale of survival. They are a valuable source of nutrients as well as a valuable method of preservation of foods. There is also much written about how our “inner ecosystems” are important for digestion and our health.

With the development of the Human Microbiome Project and other research projects by scientists related to microbes, I look forward to better understanding how fermented foods may have also helped shape human evolution. As researchers have argued, microbes may be just as important as genes in driving evolution, the human microbiome as important as the human genome. In addition, if we were to take a cue from those scientists who believe that the use of fire and cooking helps explain how we were able to grow bigger brains while shrinking our guts, it’s logical to believe that fermented foods may have had their place as well in the shaping of modern humans.

One thing that’s plainly clear is that dietary change (or change in nutrient availability) plays a heavy role in natural selection apart from climate and geographical change. Evolutionary biology is rich in examples of animals relying on bacteria to supply important nutrients in their diets. These are classic cases of higher organisms “delegating” responsibility of digestion or nutrient production to lower organisms. What I find intriguing is learning how much the interaction with bacteria may have guided natural selection in shaping morphological and physiological traits as well as behaviors of different animals including ourselves.

References

  1. Bellier R, Gidenne T, Vernay M, & Colin M. In vivo study of circadian variations of the cecal fermentation pattern in postweaned and adult rabbits. J Anim Sci 73(1):128-35.
  2. Hooper DC, Alpers DH, Burger RL, Mehlman CS, Allen RH. J Clin Invest 1973 December; 52(12): 3074–3083. doi: 10.1172/JCI107506
  3. Scott R, Sullivan WC. Ecology of Fermented Foods. Research in Human Ecology 2008;15(1):25-31. 
  4. Yatsunenko T, Rey FE, Manary MJ, Trehan I, Human gut microbiome viewed across age and geography Nature 486, 222–227 (14 June 2012) doi:10.1038/nature11053

Why aren’t we talking about organic GMOs? And, why can’t we all get along?

What I want to ask is this: Why aren’t there more people, beyond scientists and academics, talking about organically grown GMOs? These last few weeks have had me thinking a lot about how the terms used to describe our food — “organic,” “conventional,” and genetically modified” — which only serve to confuse and distract from greater issues at hand.

The greater issues (in a nutshell): Agricultural and food scientists are given a heavy task of feeding nine billion people by 2050. Most will agree that it will come with substantial costs. Soil quality will suffer, excess pesticide and herbicide use will destroy biodiversity, nutrient runoff will keep fueling the algal booms, or “dead zones,” that suffocate life in our lakes and oceans. The world’s phosphorus reserves will be depleted. If you add in climate change to the mix, you can count on destroyed crops and suffering farmers, especially in the developing world. Food production will be more expensive. Food will be more expensive. Small farmers and the poorest among us will suffer.

Organic is not the answer, but offers lessons

“Organic” farming defined as it is now is not the answer. Scientific American blogger Christie Wilcox (@nerdychristie) deserves high praise for shattering myths about organic foods and for challenging their use as being better for the environment. She also rightly challenges the notion that organic pesticides are healthier or that fewer pesticides overall in food are healthier for you. (I’ll add that some pesticides are good for you including my favorite: caffeine!).

Huge limitations are that organic agriculture requires more land and more labor. Organic agriculture also excludes synthetic pesticides (natural ones are not as effective and not safer) and herbicides aren’t permitted (despite that ones like glyphosate degrade rapidly in soil). Organic farming is, thus, more expensive and more devastating to the environment because of increased carbon emissions. And, although reports vary widely, yields of organic agriculture are also estimated to be only half in comparison to conventional agriculture.

Yet the ideals of organic agriculture are still good — less use of pesticides, herbicides, and fertilizers while protecting soil. There are also lessons to be learned from organic agriculture. For example, crop rotation can help prevent nutrient depletion in soil. And, the use of animal manure and decaying plants instead of commercial fertilizer helps improve water-holding capacity of soil. Better water-holding capacity diminishes runoff.

Bringing in biotech

Now, allow me to get back to my argument and questions — What if we added biotechnology to the picture? Why not organically grown GMOs, legislation to support expanding “Certified Organic” to include GMOs, and investment and research into more sustainable GMOs?
Finally, what if more of the public learned to appreciate the very scientists who are trying to make these developments possible? Too few people are familiar with (and too few companies have invested in) important research using recombinant DNA going on right now that could surely help reduce the impact of agriculture on the environment. For example,
  • There are the scientists researching varieties of wheat genetically engineered to emit a non-toxic pheromone, which could lead to less use of pesticide.
  • There are the scientists who’ve engineered rice to have larger root systems that take up more nitrogen and phosphorus from the soil, which reduces nutrient runoff.
  • There are the scientists whose research involves improving abilities of crops to capture more light (improving yields), withstand extreme weather changes, high salt concentrations, or have greater resistance to diseases.
  • There are also the scientists whose research is in genetically engineered algae that can help displace use of corn ethanol and petroleum while sucking carbon dioxide out of the atmosphere.
  • And, there are the scientists who actively promote this kind of research and thinking such as plant geneticists Pamela Ronald, of UC Davis, and Nina Fedoroff, of Penn State.
Currently, public perception and debate hinders the discussion of organic GMOs. Most lay people that I talk to appear to be only familiar with stories of either poor behavior from GMO-corporations like Monsanto, or their Roundup Ready crops as a source of overuse of fertilizer and pesticide, the destruction of biodiversity through expanded use of monoculture crops, and the spread of pesticide-resistant weeds. (Unfortunately, they are also familiar with the bat-shit crazy Jeffrey Smith, Mercola, and Mike Adams).
 
What about conventional ag and food technology?
Let’s not leave out “conventional” agriculture. There are also solutions to gain from developments in conventional agriculture, too. Too few people know about the new developments because ideologies tend to trump the science and technology. Yet a couple of years ago, food scientists from a variety of disciplines produced a scientific review on behalf of the Institute of Food Technologists that offered these solutions:
  • “No-till” agriculture – retains organic matter and stops soil erosion
  • Integrated pest management – using pesticide only where it’s needed, decreasing amount
  • Precision agriculture – targeting fertilizer to seed, pesticide to plant
  • Drip irrigation – controlling water
  • New technologies for recovering nitrogen and phosphorus from wastewater (like Bill Gates toilets)

I’ll also add in food technology. Despite the massive criticism received by food technologists (“Big Food”) for fueling the obesity epidemic, it will be their task for providing additional food processing solutions to feed the world’s nine billion.

For example, there are many improved technologies for preserving food and extending shelf life of these foods. The technologies we have now (besides cooking) are mechanical operations (extraction and separation of oils), thermal treatments (blanching, pasteurization, and canning), refrigeration, dehydration, fermentation, acidification, etc. New technologies like faster thermal methods (microwave and ohmic heating) and high-pressure processing could help feed people in the future.

Controlled-environment agriculture looks promising, too; that is, the designing of high-tech greenhouses that can be produced almost anywhere, including Antarctica, and can produce up to 10 times more produce than conventional farms with only a tenth or less of the resources. Cost is the prohibitive factor there.

A Unified Approach

So, why the dividing lines? Excluding GMOs from the label of “Certified Organic” is based in ideology and not in science. Too many people have it in their minds that GMOs are “anti-organic.” It doesn’t have to be that way. Food labeling of GMOs does little to solve this problem, but only discourages investment into biotechnology and its commercialization. The “Certified Organic” labeling also distracts from focusing on the progress that biotechnology and other technologies offer for more sustainable, environmentally friendly practices.

Catastrophe has been avoided before. In the 1960s and ’70s, population growth outpaced food production. Bringing science to agriculture turned the tables and improved plant breeding techniques, which increased yields of common crops like wheat. Thanks to scientists like Norman Borlaug (and Fritz Haber, for that matter), the Green Revolution saved millions, mainly in China and India.

It can happen again. The goals shared should be improving crop yields in harsh environments, reducing nutrient runoff, reducing use of pesticides and herbicides, and reducing food waste and pollution through a combination of the best that organic, GMOs, and conventional techniques have to offer. There simply needs to be a more unified approach to improving food production and reducing its impact on the environment.

Update 09-26-12: And, about that flawed rat study everyone’s talking about, I believe plant scientist Peter Bickerton beautifully summarizes my own thoughts, over on the “Topical Poetry” blog, with this masterpiece. Enjoy!

Making lazy, stupid plants work harder

Plants with larger root systems take up minerals more easily.

Plants these days. They’re coddled, entitled, fed with a silver spoon.

Use of man-made fertilizer and traditional breeding, over the years, has selected for traits that led to today’s modern-variety plants that grow fat with yields.

But the downside of easy access to nutrients is that it has allowed for the breeding out of desirable traits that has left plants, well, acting like enabled, spoiled children.

“They’re lazy,” said plant biochemist Roberto Gaxiola, an assistant professor of cellular and molecular biosciences at Arizona State University. Because nutrients are plentiful, they don’t bother with growing large root systems. Yet, he explained to me, larger root systems are needed for them to take up more phosphate and nitrogen from the soil.

More now than ever, plants depend on these fertilizers for growth. Wild crop plant varieties, on the other hand, have had to evolve in an environment of everyday nutrient scarcity. It’s these wild crop plant root systems that have been the focus of Gaxiola’s research for more than a decade.

Root engineering 

Gaxiola told me that these wild varieties have learned to use more efficient pathways of transporting sugars from leaves to roots. They produce larger root systems that do a better job at acidifying soil and taking up minerals like nitrogen, phosphate, potassium.

He’s identified genes involved in overexpression of a type of kinase, an H+-PPase, that phosphorylates a process of loading sugar. The localization of this kinase is in cells that surround the vascular tissue, which is used to synthesize and transport sugar.

“It’s the only way that roots can grow and be active,” Gaxiola told me. “You cannot grow a root if you don’t move sugar from the leaves. What does this kinase regulate? It could be one of the genes, but clearly it’s multifactorial. It’s upregulating sugar transport for a larger root system.”

Last May, Gaxiola and his colleagues published their latest of a series of papers detailing how his lab inserted genes from wild rice, tomatoes and arabidopsis into modern-yield, salt-tolerant varieties (1). These genes, as part of commercial varieties through root engineering, could lead to more efficient use of phosphorus and increase crop biomass and seed yields.

Another paper, recently published in Nature by scientists from the International Rice Research Institute, uses a similar approach (2). These scientists isolated and inserted a gene from a wild variety of rice into commercial strains to produce larger roots that better take up phosphorus, nitrogen, and potassium.

Gaxiola said, “It’s interesting work. We have similar results, but with a different gene.” Again, a kinase is involved that regulates synthesis of sugar for transport to the roots to become more active, grow, and take up minerals.

Phosphorus and the future

“It’s a good example of how crop domestication made crop plants ‘stupid’ and dependent on heavy external fertilizer inputs. Their plants seem very promising indeed,” said biologist James Elser, a subject of a previous post.

Elser, also an ASU professor, is raising more awareness about the need for sustainable phosphorus. His wish, he’d said to me before, is to hear “President Obama say the word ‘phosphorus’,”as the problem deserves serious attention.

According to Elser, plants that can more efficiently use phosphorus could end up being highly beneficial to poor people, such as in underdeveloped Asian countries. As phosphorus availability becomes depleted and costs for fertilizer rises, farmers in these countries can’t afford fertilization of their rice plants. They’re also hit with the fact that the roots won’t take nutrients. Often the soils have the phosphates, but they’re bound to the soil. The roots need to acidify the soil to release the phosphate that’s bound.

Plants that efficiently use phosphorus could also reduce eutrophication. The problem is caused when fertilizer run-off enters streams, rivers, lakes, and oceans. These extra nutrients cause algae to bloom and create “dead zones,” Elser said, one of the most famous examples of which is the Gulf of Mexico Dead Zone.

Hurdles of funding and anti-GM sentiment

With so much to gain from plants that can grow in phosphorus-poor soil or with less fertilizers, I had to ask Gaxiola, How close are we to seeing salt-tolerant, large-rooted plants being used commercially? Gaxiola’s plants, for example, as he described, are “one of the strongest phenotypes” ever produced for the market.

“Oh, my friend,” Gaxiola replied gently to my question, in a way I’ve found to be typical of his native Mexico City, “there are field trials, heavy investment, and then you have to pray that a company like Monsanto gets interested.”

Why Monsanto? Because there are few other large biotechnology companies who could jump through the hoops required to commercialize a genetically engineered crops. It’s unfortunate, Gaxiola told me, because to reduce the impact of fertilizer overuse on the environment and biodiversity, what we really need is more investment into plant engineering and more commercialization of nutrient-efficient plants.

One is led to wonder: With all it’s focus on growing crops organically, is anti-GM sentiment actually hindering development of plants that could help the environment? Also, who is anti-GM sentiment helping if not only Monsanto? If only Monsanto can invest in GM? Wouldn’t less regulations on GM help other biotechnology companies get in the game? These are questions worth more exploration.

References

  1. Gaxiola RA, Sanchez CA, Paez-Valencia J, Ayre BG, Elser JJ. Genetic Manipulation of a “Vacuolar” H+-PPase: From Salt Tolerance to Yield Enhancement under Phosphorus-Deficient Soils. Plant Physiol 159, 2012;3-11. doi: 10. 1104/ pp. 112. 195701
  2. Gamuyao R, Chin JH, Pariasca-Tanaka J, Pesaresi P, Catausan S, Dalid C, Slamet-Loedin I, Tecson-Mendoza EM, Wissuwa M, Heuer S. The protein kinase Pstol1 from traditional rice confers tolerance of phosphorus deficiency. Nature 488, 535–539 (23 August 2012) doi: 10.1038/nature113466

Photo credit: ASU

Calcium: U.S. adults still not getting enough

A new study suggests most U.S. adults continue to fail to get enough of the mineral through diet and supplementation to meet recommended levels.

University of Connecticut and Yale University researchers examined data from National Health and Nutrition Examination Survey collected from 9,475 adults between 2003 and 2006. They found that, although dietary calcium intake was reported highest in older age groups, the amounts remained insufficient to meet adequate intake standards for age groups 50 years and older.

These inadequate intakes come despite the fact that more than half of individuals ages 19 and older were taking a calcium supplement, according to the authors. For men, supplementation increased from 34 percent in the 19 – 30 age group to 54 percent in the 81 and older age group. The percentage of women taking supplements rose from 42 percent to 64 percent across the same range of age groups.

“Adequate lifelong calcium intake is essential to optimizing bone health,” remind the study authors, who published their findings in the May 2011 issue of Journal of American Dietetic Association. They also recommend “new approaches to increasing the frequency and level of calcium supplement use to enhance calcium density in diets.”

Calcium is the most abundant mineral in the body, primarily found in the bones and teeth. As bones develop, calcium, along with other minerals, crystallizes on the collagen matrix of the bone, making it denser and giving it strength and rigidity. The body loses calcium continuously, and if this loss is not replaced through diet, the body will remove calcium from the bones to perform necessary functions such as regulation of muscle contraction. This removal causes bones to become soft and brittle, making them prone to fractures.

Adequate calcium intake is necessary for strong and healthy bones. The current recommended intake of calcium is between 1,000 mg and 1,300 mg per day. Good sources (more than 300 mg per serving) of calcium include dairy products such as low-fat milk, cheese, and yogurt. Dark green vegetables such as broccoli, kale, and spinach can also add about 90 milligrams of this mineral to daily intake. In addition, calcium-fortified foods (orange juice and breakfast cereals) and dietary supplements can also help fill gaps.
Other important factors in optimizing bone health include engaging in weight-bearing exercise and obtaining recommended amounts of vitamins D and K2 daily.

Reference: Mangano KM, Walsh SJ, Insogna KL, Kenny AM, Kerstetter JE. Calcium Intake in the United States from Dietary and Supplemental Sources across Adult Age Groups: New Estimates from the National Health and Nutrition Examination Survey 2003-2006. J Am Diet Assoc 2011;111:687-95.

Thoughts:

Time and time again, studies have shown that calcium when combined with vitamin D are effective in increasing bone density. However, there’s been a lot of back and forth in the calcium world around the topic of supplements, particularly their efficacy and safety. A critical piece lacking in the conversation is of absorption since calcium is one mineral that depends on a few factors — vitamin D, doses that oversaturate absorption, too much absorbed at once.

The best approach for obtaining calcium is perhaps to consume it as we would have back in the time of our hunter-gatherers ancestors before the agricultural revolution and pastoralism, which is by getting a little here and a little there when we only obtained it from the leaves of plants. That’s not to say that we should only get it from plant leaves, but that we should get it in smaller amounts in sustained fashion over the course of a day.

Fusing aging theories: Telomere shortening causes mitochondrial dysfunction

New research is adding insight and linking three theories of aging—one that suggests telomere shortening governs lifespan, and two others that suggest dysfunctional mitochondria or oxidative stress leads to aging.

At Harvard-affiliated Dana-Farber Cancer Institute, scientists have gathered data suggesting telomere shortening is the cause of mitochondrial dysfunction and diminished antioxidant defenses. Together, they decrease the body’s energy and diminish organ function, both characteristic of old age.

As telomeres—protective caps at the end of cell chromosomes—shorten with age and begin to fray, cells activate the p53 gene, which signals an “emergency shutdown” chain of events that turns off normal cell growth and division and compromise antioxidant defenses. Going one step further, data from the carefully orchestrated mouse study, published in Nature, show that the p53 gene also represses PGC1-alpha and PGC1-beta. These PCGs are considered the master regulators of metabolism and mitochondrial function.

Repressing PCGs increases the number of dysfunctional mitochondria (with mutated mitochondrial DNA) and leads to a decrease in functional mitochondria distributed throughout in muscles and organs. The dysfunctional mitochondria in aged tissues leak greater amounts of reactive oxygen species and the lack of functional mitochondria hinders normal energy production from cell respiration (the body’s main producer of ATP energy).

“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent from each other,” said Ronald A. DePinho, M.D., a cancer geneticist and senior author of the paper, in a press release.

“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” Dr. DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”

In an article also published in the same issue Nature, Daniel P. Kelly, M.D., scientific director and professor at Burnham Institute for Medical Research-Lake Nona, Orlando, Florida, said that the “intriguing study… unveils a potentially unifying mechanism for cellular ageing.”

Mitigating the Toll of Aging

The new study further supports current thinking that the best defense against aging is to reduce the adverse affects of overproduction of free radicals produced from dysfunctional mitochondria, which cause additional oxidative stress.

Dr. DePinho said, “The findings bear strong relevance to human aging, as this core pathway can be directly linked to virtually all known genes involved in aging, as well as current targeted therapies designed to mitigate the toll of aging on health.”

Those current targeted therapies include boosting the human body’s antioxidant defenses by eating a healthy diet, reducing calories (by around 25 percent), and supplementing with antioxidant vitamins C and E, as well as with green tea, CoQ10 and resveratrol. These practices not only help to protect against oxidative stress, thereby protecting against telomere shortening, but also help boost generation of new, healthy mitochondria.

When we asked telomere biologist Bill Andrews, Ph.D., to comment on the new study, he answered that it was “tremendous news,” as it supports the need for more research into management of telomeres by activating the genetic expression of the enzyme telomerase, which re-lengthens telomeres.

Dr. Andrews wrote, “It’s the best support ever for the fact that telomere elongation’s role in aging far exceeds the roles played by mitochondria and oxidative stress.” In effect, telomere shortening is the root cause of the others.

Mitochondria become dysfunctional when telomeres shorten and fray, a new study suggests. In an article to be published in a forthcoming issue of IsaNews magazine, Dr. Andrews writes, “Mitochondrial dysfunction causes aging—but telomere shortening has turned out to be the primary cause of mitochondrial dysfunction. And humans’ natural defenses against oxidative stress are really quite exceptional (for example, our cells produce ten times more superoxide dismutase, a potent natural antioxidant, than mice)—until telomere shortening begins to degrade those defenses inside our bodies.”

He added that while “anti-aging therapies of years past merely treated the symptoms of aging. New research is devoted to identifying a new class of therapies that treat aging at its root cause, and hold great promise of one day allowing us to feel young and healthy at 120 years of age and beyond.”

An earlier study, of which Dr. DePinho was also the senior author, gives testimony to the benefits of telomerase, as found in mice that were genetically engineered to produce the enzyme. The study found that when the telomerase was restored in the mice, their age-related symptoms disappeared and several organs including the brain were rejuvenated.

References:

Kelly DP. Cell biology: Ageing theories unified. Nature 2011;470:342-3.

Sahin E, Colla S, Liesa M et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470:359-65.

Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature 2010;464:520-8.

Jaskelioff M, Muller FL, Paik JH et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011;469:102-6.

The Nature of Human Skin Pigmentation

Nina Jablonsky

On Sunday morning at #AAASmtg in Washington DC, Nina Jablonski talked to use about human skin pigmentation as an example of natural selection.

“Human skin is colorful, it’s mostly naked, it’s sweaty, and it’s tough yet sensitive,” Jablonski said. The gradient of human skin pigmentation is very clear in the old world, as it’s lighter in the northern countries and darker in Africa.

But why did human skin pigmentation evolve as it did? When you look at other apes and humans, our relatives have lightly pigmented skin covered by dark hair — this was the ancestral pigmentation of our lineage.

“When you think of Lucy’s species, you can think of lightly pigmented skin covered by dark hair,” she said, noting that eventually as the hominins became more naked they developed more melanin.

When Homo ergaster 1.6 mya was foraging in the savannah, the species would have needed more naked and sweaty skin for keeping cool. In addition, Jablonski’s research has found that permanent dark pigmentation evolved 1.2 mya, at the same time as these other developments — an interesting development!.

Exposed skin could lead to disease states, so by increasing the amount of pigmentation, H. ergaster protected the species and the pigmentation was selected on.

Ultraviolet radiation (UVR) had a lot to do with the advent of darker skin pigmentation. On a map (by George Chaplin based on NASA TOMS7 satellite data) of annual average UVR, Jablonski was able to clearly show the strength of UVR.

“We evolved initially in equatorial Africa and then we had two waves of dispersal from Africa,” Jablonski said. “This really changed the selective genes for human skin fundamentally.”

The key thing about ultraviolet radiation is that wavelengths do different things to the human body. In general, UVR does a lot of damage, such as DNA damage leading to skin cancer.

Skin cancer generally affects people as they’re older beyond their reproductive years. However, the sun has a definitive effect on folate metabolism. One of the key things we see as important, is the effect on folate metabolism on birth defects. Because folate is needed for making DNA and the competition for folate is intense in the presence of UVR,  “why not increase the amount of melanin — a superb natural sunscreen — the evolution of permanent melanin was extremely important in high equatorial radiation levels.”

However, melanin comes with a downside. It slows production of vitamin D precursor in the skin, which is essential for calcium metabolism and bone health, as well as incredibly important to the maintenance of a strong immune system.

If we look at our hairy timeline, 6 mya we had hair and light skin, then with dispersal from Africa into India and Asia, then eventually Indonesia and Europe, what did UVR have as an influence?

To Jablonski, it is the combination of needing to protect against DNA damage and folate metabolism as much as possible, but while naturally selecting for less skin pigmentation for keeping the skin light enough to absorb enough UVB rays to create vitamin D.

Indeed, we have an independent evolution of depigmentation of humans in Asia and in Europe. And we also know that the Neandertals experienced the same selection of depigmentation. There are many genes involved in pigmentation and Jablonski said she has even found in some populations, where the amount of UVR changes by season, that people have adapted to change the amount of melanin in their skin throughout the season

Nowadays, accelerated rates of movement around the world, has put humans in environments that are poorly matched, Jablonski said, which has created serious health problems such as with rickets in children, birth defects, and even metabolic syndrome.

For the purposes of education on health, we need to teach that skin color is an adaptation. It is the most visible product of evolution by natural selection on the human body. This is why we need to use it to teach evolution, Jablonski said.

Additional note posted Tuesday, Feb 22. I discovered afterward that Jablonski has a wonderful TED talk that I think everyone should watch, so I posted it below.

How much vitamin C do you really need?

Note: Vitamin C is fascinating topic and there’s no better way to understand it than through the eyes of my boss, Dr. Rockway. I’m glad I had the pleasure of editing her article and posting it here. David

By Susie Rockway, Ph.D.

Vitamin C, or ascorbic acid (ascorbate), is the most frequently taken dietary supplement in North America. Yet, despite its widespread use, national surveys report that 15 percent of the population still doesn’t get enough vitamin C to meet recommended amounts for health.

Initially, the Recommended Daily Intake (RDI) for vitamin C was set at 60 milligrams, the amount required to prevent scurvy. The deficiency disease—commonly characterized by bleeding gums and loosened teeth helped identify the vitamin as having an essential role in collagen formation.

However, more recent research has now made it clear that more dietary vitamin C is needed to saturate body tissues such as the brain, heart, liver, and adrenal glands.

Consequently, in 2000, the RDI was raised to 90 and 75 milligrams daily for men and women. The new values were based on studies suggesting that plasma vitamin C should be maintained at specific levels (~80 µmol/L) for good health and antioxidant activity.

This is how the “debate on how much of vitamin C is needed” began—with scientists discussing two questions:

  • How much vitamin C is really needed to make an impact on plasma levels?
  • Are plasma levels really the best indication of tissue saturation levels?

Of Mice and Vitamin C

While there is still not any consensus on this matter, a new, carefully designed study just published in the February issue of American Journal of Clinical Nutrition provides some clues for answering these questions.

In the study, New Zealand researchers compared “normal” mice vitamin C tissue saturation levels with “knockout” mice that were genetically engineered to lack the enzyme needed for synthesizing vitamin C in the body.

Without dietary vitamin C, they saw that tissue concentrations of ascorbate became deficient weeks before the onset of scurvy symptoms in the mice, similar to humans. During these weeks, the scientists observed that the mice exhibited signs of impaired collagen synthesis, changes in aortic wall structure, formation of atherosclerotic plaque, and activation of inflammatory processes.

Sustaining Tissue Concentration

The scientists observed that each tissue became deficient at different rates. For example, the brain maintained its vitamin C longer than other organs; however, after just two weeks of deficiency, vitamin C in the brain became depleted. To replenish these tissues to normal levels, plasma concentration had to be maintained saturated with daily ascorbate intakes.

In addition, they found that tissue levels of ascorbate became saturated more quickly when the mice ate kiwi fruit versus sodium ascorbate in water—the flavonoids present in kiwi are thought to enhance absorption of vitamin C by maintaining it in a reduced state (versus an oxidized state).

Lastly, based on the new evidence, the researchers wrote that the current RDI should receive no less than a 60 percent boost—from 75 milligrams per day to at least 120 milligrams per day—to keep not only plasma levels saturated, but also tissue levels of the brain, and organs that are unable to be measured with current methods.

The vitamin C researchers stressed the need for people to maintain an ongoing and constant vitamin C intake to sustain tissue concentration—which means consuming the scientists’ recommended amounts regularly.

What Weight Has to Do with Vitamin C

Another less well-known role of vitamin C is its involvement as a cofactor in the biosynthesis of carnitine, a molecule required for burning fat as energy fuel (fatty acid oxidation).

Interestingly, there is a direct inverse relationship with obesity (adiposity) and plasma vitamin C concentrations—as plasma ascorbate levels are decreased, fatty tissue increases (adiposity increases).

This association has led researchers to wonder whether or not decreased vitamin C levels cause less carnitine to be synthesized and if there is a relationship between less carnitine and less burning of fat for fuel.

Preliminary findings are that subjects who are vitamin C depleted have lower levels of carnitine leading to a 25 percent decrease in fatty acid oxidation (per kilogram body weight) than individuals whose vitamin C status is adequate.

The researchers speculate that reduced fat oxidation seen with vitamin C depletion may result in weight gain by two mechanisms:

  • Indirectly, decreased carnitine leads to increased fatigue during exercise and this may lead to exercise intolerance
  • Directly, by lipid (fat) accumulation

The prevalence of obesity in the world currently has led researchers to suggest that more attention is needed to the problem of vitamin C deficiency affecting at least 15 percent of the population, if not more.

Sources

  1. Vissers MCM, Bozonet SM, Perason JF and Braithwaite LJ. Dietary ascorbate intake affects steady state tissue concentrations in vitamin C-deficient mice: tissue deficiency after dietary ascorbate intake affects steady state tissue concentrations in vitamin C-deficient mice: tissue deficiency after suboptimal intake and super bioavailability from a food source (kiwifruit). AJCN 93(2):292-301, 2011.
  2. Johnston CS, Corte C and Swan PD. Marginal vitamin C status is associated with reduced fat oxidation during submaximal exercise in young adults. Nutr & Metab 3(35):1-5, 2006.