The China Study II: A look at mortality in the 35-69 and 70-79 age ranges

This post is based on an analysis of a subset of the China Study II data, using HealthCorrelator for Excel (HCE), which is publicly available for download and use on a free trial basis. You can access the original data on the HCE web site, under “Sample datasets”.

HCE was designed to be used with small and individual personal datasets, but it can also be used with larger datasets for multiple individuals.

This analysis focuses on two main variables from the China Study II data: mortality in the 35-69 age range, and mortality in the 70-79 range. The table below shows the coefficients of association calculated by HCE for those two variables. The original variable labels are shown.

One advantage of looking at mortality in these ranges is that they are more likely to reflect the impact of degenerative diseases. Infectious diseases likely killed a lot of children in China at the time the data was being collected. Heart disease, on the other hand, is likely to have killed more people in the 35-69 and 70-79 ranges.

It is also good to have data for both ranges, because factors that likely increased longevity were those that were associated with decreased mortality in both ranges. For example, a factor that was strongly associated with mortality in the 35-69 range, but not the 70-79 range, might simply be very deadly in the former range.

The mortalities in both ranges are strongly correlated with each other, which is to be expected. Next, at the very top for both ranges, is sex. Being female is by far the variable with the strongest, and negative, association with mortality.

While I would expect females to live longer, the strengths of the associations make me think that there is something else going on here. Possibly different dietary or behavioral patterns displayed by females. Maybe smoking cigarettes or alcohol abuse was a lot less prevalent among them.

Markedly different lifestyle patterns between males and females may be a major confounding variable in the China Study sample.

Some of the variables are redundant; meaning that they are highly correlated and seem to measure the same thing. This is clear when one looks at the other coefficients of association generated by HCE.

For example, plant food consumption is strongly and negatively correlated with animal food consumption; so strongly that you could use either one of these two variables to measure the other, after inverting the scale. The same is true for consumption of rice and white flour.

Plant food consumption is not strongly correlated with plant protein consumption; many plant foods have little protein in them. The ones that have high protein content are typically industrialized and seed-based. The type of food most strongly associated with plant protein consumption is white flour, by far. The correlation is .645.

The figure below is based on the table above. I opened a separate instance of Excel, and copied the coefficients generated by HCE into it. Then I built two bar charts with them. The variable labels were replaced with more suggestive names, and some redundant variables were removed. Only the top 7 variables are shown, ordered from left to right on the bar charts in order of strength of association. The ones above the horizontal axis possibly increase mortality in each age range, whereas the ones at the bottom possibly decrease it.

When you look at these results as a whole, a few things come to mind.

White flour consumption doesn’t seem to be making people live longer; nor does plant food consumption in general. For white flour, it is quite the opposite. Plant food consumption reflects white flour consumption to a certain extent, especially in counties where rice consumption is low. These conclusions are consistent with previous analyses using more complex statistics.

Total food is positively associated with mortality in the 35-69 range, but not the 70-79 range. This may reflect the fact that folks who reach the age of 70 tend to naturally eat in moderation, so you don’t see wide variations in food consumption among those folks.

Eating in moderation does not mean practicing severe calorie restriction. This post suggests that calorie restriction doesn't seem to be associated with increased longevity in this sample. Eating well, but not too much, is.

The bar for rice (consumption) on the left chart is likely a mirror reflection of the white flour consumption, so it may appear to be good in the 35-69 range simply because it reflects reduced white flour consumption in that range.

Green vegetables seem to be good when you consider the 35-69 range, but not the 70-79 range.

Neither rice nor green vegetables seem to be bad either. For overall longevity they may well be neutral, with the benefits likely coming from their replacement of white flour in the diet.

Dietary fat seems protective overall, particularly together with animal foods in the 70-79 range. This may simply reflect a delayed protective effect of animal fat and protein consumption.

The protective effect of dietary fat becomes clear when we look at the relationship between carbohydrate calories and fat calories. Their correlation is -.957, which essentially means that carbohydrate intake seriously displaces fat intake.

Carbohydrates themselves may not be the problem, even if coming from high glycemic foods (except wheat flour, apparently). This post shows that they are relatively benign if coming from high glycemic rice, even at high intakes of 206 to 412 g/day. The problem seems to be caused by carbohydrates displacing nutrient-dense animal foods.

Interestingly, rice does not displace animal foods or fat in the diet. It is positively correlated with them. Wheat flour, on the other hand, displaces those foods. Wheat flour is negatively and somewhat strongly correlated with consumption of animal foods, as well as with animal fat and protein.

There are certainly several delayed effects here, which may be distorting the results somewhat.  Degenerative diseases don’t develop fast and kill folks right away. They often require many years of eating and doing the wrong things to be fatal.

Losing weight without developing gallstones

Gallstones are estimated to affect 1 in 10 people in North America. Those who are obese have a higher likelihood of developing gallstones. Most at risk of gallstones as a result of obesity are Native Americans, the elderly, and Caucasian women in their forties who haven’t yet reached menopause.

Gallstones are so named because they develop in the gallbladder, a small organ that stores and releases the bile made by the liver. Bile is a dark green fluid containing bile salts and cholesterol. The gallbladder releases bile into the small intestine to assist in digesting fats more efficiently. However, if the bile contains high concentrations of cholesterol, then stones too difficult for the bile salts to dissolve may develop.

Because gallstones usually form without any symptoms, most people don’t know they have them or may feel only minor symptoms such as abdominal pain after eating a fatty meal. However, if a stone becomes lodged in a bile duct causing blockage, it can result in sudden pain in the abdomen, back or right shoulder.

Cholecystitis, or gallbladder disease, which is caused by duct blockage, infection or inflammation, is one of the most common digestive diseases. Pain from duct blockage can become intense and lead to hospitalization and surgery. In the U.S. alone, gallbladder surgeries approach 700,000 annually, costing approximately $6.5 million.

Surgery costs increase if gallstones and duct blockage or infection cause the pancreas to become inflamed. The resulting pancreatitis can lead to severe or life-threatening complications. The major cause of acute pancreatitis in North America is gallstones.

Link to Obesity and Losing Weight Too Quickly

Because of obesity’s major role in the formation of gallstones, weight management is critical for decreasing the likelihood of developing them. Obesity is thought to increase risk of gallstones because of elevated production of cholesterol, which in turn increases the concentration of cholesterol in bile.

Paradoxically, losing weight actually increases risk of developing gallstones among obese people, especially amongst those who lose large amounts of weight rapidly. Although not entirely understood, nutritional and medical scientists think that losing weight too quickly may shift the balance of bile salts and cholesterol, causing increased concentrations of cholesterol. Gallstone risk may also be increased by consuming a diet too low in fat or avoiding fat, which reduces the frequency of gallbladder contractions and results in fewer chances of gallbladder emptying.

As always, individuals with a high risk for gallstones should follow medical advice in treatment. Medical researchers have studied methods that obese people can lose weight while reducing risk of gallstone developments. Statin regimens and bile salt therapies have had mixed results. A drug called ursodiol has shown much promise in helping to dissolve cholesterol in bile and prevent gallstones.

There have also been successes such as employing modifications in diet to help reduce risk of gallstones. Along with following a doctor’s advice, individuals can consider these weight-management strategies, which have shown promise based on epidemiologic studies or in clinical trials for losing weight as naturally and safely as possible.

Three Steps to Help Lower Risk of Gallstones While Losing Weight

Step 1: Avoid very low-calorie dieting, losing no more than 1-2 pounds per week.

Overall, research studies have found that obese people who lost 3 pounds or more weekly had a greater likelihood of developing gallstones. This may be because they are more likely to experience an imbalance between bile salts and cholesterol, as well as irregular gallbladder emptying.

For these reasons, people who are obese or who are at high risk for developing gallstones should also avoid skipping meals or fasting.

By eating three steady meals throughout the day and losing weight at a slower rate, obese people can reduce the weight-loss risk factor in gallstone formation. To ensure steady weight loss at 1-2 pounds per week, calorie intake should be reduced by only 500 to 1,000 calories. Weight loss is also influenced by activity, which may require eating more calories to compensate for calories burned.

Step 2: Avoid saturated fats and eat small amounts of monounsaturated or polyunsaturated dietary fat daily.

Foods high in saturated fats, trans fats and cholesterol are all associated with increased risk in gallstone formation. However, foods high in polyunsaturated or monounsaturated fats (from olive oil or high-oleic sunflower oil) may help lower cholesterol saturation and reduce risk of gallstone formation.

A randomized clinical trial on obese subjects compared a low-calorie diet (900 kcal/d) with 30 grams of fat per day with a low-calorie diet (520 kcal/d) with less than 2 grams of fat per day. After eight weeks, not one of the subjects on the diet with 30 grams of fat per day had developed gallstones. The researchers were led to conclude that dietary fat ensured regular gallbladder emptying and reduced bile cholesterol saturation.

A 10g threshold of fat per meal is now considered to be most efficient at maximizing gallbladder emptying, which can support healthy weight loss while reducing risk of formation of gallstones.

Furthermore, according to one randomized, double-blind, placebo-controlled clinical trial, fish oil in amounts of almost 12 grams per day may work comparatively to ursodiol in reducing risk of gallstone formation in low calorie diets.

Step 3: Avoid refined sugar and strive for a diet high in fiber.

In epidemiologic studies, there is a higher association of gallstones in those who ate greater amounts of refined sugars. In contrast, long-term consumption of relatively high amounts of dietary fiber has been correlated with reduced risk of gallstone diseases.

The risk appears to be even lower if the amount of fiber consumed comes from sources rich in insoluble fiber found in whole grains, fruits and vegetables. Soluble dietary fiber such as found in oats and legumes also appears to be protective, showing reduction of gallstone formation in animal studies.

Diets higher in fiber and lower in refined sugars will also assist in weight loss. Refined sugars, found in high amounts in sodas and desserts, contribute to high calorie intake, which contributes to obesity. Dietary fiber is filling, providing a satiety effect, but offers little or no calories that would contribute to weight gain.

Individuals should increase dietary fiber to recommended levels (25 to 30 grams daily) gradually.

Safe Road to Optimal Health

Once again, each of these steps is a natural dietary habit that will help lower the risk of developing gallstones and support losing weight safely. Apart from diet, getting regular exercise daily is also helpful. And, for every pound lost gradually, the ultimate achievement is reduced risk of gallstones in the future.

Beyond reduced risk of gallstones, the end-benefits of healthy weight management are profound including improved activity and mobility, improved health of organs such as the heart and brain, and reduced risk of diseases such as type 2 diabetes and cardiovascular disease. Healthy weight management improves overall health and wellness at every level.

No evidence of dairy and heart disease link

New research has once again confirmed after systematically analyzing 17 studies that there is simply no evidence to substantiate claims of a link between dairy and higher risk of cardiovascular disease or death.

The evidence, in fact, shows just the opposite—drinking milk slightly reduces the risk of coronary heart disease (1). In addition, multiple studies show that milk and dairy proteins (whey and casein) may actually protect the heart by helping to maintain lower blood pressure, lower blood sugar, and lead to reduced bodyweight (2-4).

The renowned, epidemiologic and nutrition researcher Walter Willet, Ph.D., and his group at Harvard, conducted this huge analysis by looking at various types of dairy intake, ranging from milk intake to total high-fat dairy products and total low-fat dairy products and correlating to risk of cardiovascular disease (CVD), coronary heart disease (CHD), stroke and all-cause mortality. This study was a meta-analysis of many prospective cohort studies in healthy men and women (4).

Although it's always a challenging task to summarize published studies' data on food intake, Willett’s group is easily recognized as having the epidemiological expertise of doing such an analysis. Results from the group's careful analysis show:

• a statistically significant inverse association between milk intake and cardiovascular disease.
• no significant relationship between CHD, stroke, and all-cause mortality (including cancer) and total dairy of all types (high-fat, low-fat)

When they examined data on total dairy products or total high-fat dairy intake there was still no impact on CHD, but these results were based on a much smaller number of studies.

A notable strength of this methodology was the use of an advanced statistical approach for trend estimation of summarized dose-response data. This method provides uniform analysis of different studies, exposure categories and range of intakes; as well as greater power using full spectrum continuous exposure data.

These data, published in the January issue of the Journal of American Clinical Nutrition, clearly show that milk intake does not lead to cardiovascular, heart, stroke or any mortality (including cancer) and may even be beneficial in reducing cardiovascular diseases.

Several mechanisms have been discussed over the years concerning the beneficial effects of low-fat dairy intake on lowering blood pressure. For example, data from the famous DASH eating plan show systolic blood pressure reduction with a healthy diet. Inclusion of low-fat dairy products or dairy proteins showed a potential anti-hypertension effect possibly due to the natural mineral content found in dairy, particularly phosphorous.

These types of studies do not show cause and effect, but do, in fact, show that there is not an increased risk of heart disease, cardiovascular disease, stroke or all-cause mortality by drinking milk. One can only hypothesize why these associations exist—a clear possibility is that milk drinkers are taking extra dietary care by consuming natural products, perhaps in place of sugar-laden soft drinks. Diet quality is the key in reducing risk of chronic disease.

CVD is the main cause of death in the Western world claiming 17 million lives each year. Since saturated fat intake is associated with heart disease, dairy foods have often been blamed for contributing to CVD; however, the science community has yet to agree because of many conflicting studies. Although most epidemiological studies have failed to show an effect of dairy on CVD, a few have shown a positive correlation.

Likely confusion arises when results from dissimilar studies get lumped together in hopes of finding the "answer." However, combining evidence from epidemiological, case-control, prospective study designs with different age groups, genders, countries and numbers of subjects may easily explain the mixed results.

References

1. Soedamah-Authu SS, Ding EL, Al-Delaimy WK, Hu FB, Engberink MF, Willet WC and Geleijnse JM. Milk and dairy consumption and incidence of cardiovascular disease and all-cause mortality: dose-response meta-analysis of prospective cohort studies. Am J Clin Nutr 2011; 93: 158-71.
2. Petersen BL, Ward LS, Bastian ED, Jenkins AL, Campbell J, Vuksan V. A whey protein supplement decreases post-prandial glycemia. Nutr J 2009;8:47.
3. Frestedt JL, Zenk JL, Kuskowski MA, Ward LS, Bastian ED. A whey-protein supplement increases fat loss and spares lean muscle in obese subjects: a randomized human clinical study. Nutr Metab (Lond) 2008;5:8.
4. Fluegel SM, Shultz TD, Powers JR, Clark S, et al. Whey beverages decrease blood pressure in prehypertensive and hypertensive young men and women. International Dairy Journal; 1010; 753-760.

...towards a m a n i f e s t o

Some thoughts on happiness...

Hedonic well-being?

Let Sunshine Win the Day
or Cynicism: it’s healthy and it makes me happy

The North West m a n i f e s t o events came about as a response to societal changes and as a way of artists and health allies expressing their frustrations and articulating shared passion. As a piece of work, it’s less about strategising and more about connecting and moving forward, and very much in the tradition of artist’s manifestos: its about shouting from the roof-tops.

Last week’s event in Liverpool was planned to give voice to practitioners across Merseyside to come together and exchange ideas and vision to inform the manifesto and celebrate some of the unfolding activity across the area. So, as part of a series of events, exploring shared aspirations for the field, this was a bit of a hybrid event, and with over fifty people in the room was vocal, buoyant and inspiring.

I introduced the session by framing our practice in relation to wider national and regional activity and placing the arts at the heart of society, both in reflection and reaction.

Artistic Director of FACT, Mike Stubbs went on to give a Liverpool context, painting a picture of a thriving and engaged cultural sector and challenging us to think about how we evidence our impact.

Punctuated with artist’s interventions, the session drew some significant thoughts and insight from participants that can be found on the dedicated m a n i f e s t o /merseyside blog pages (only available to that sessions participants, but all the m a n i f e s t o sessions will be drawn together leading up to June 2011).

The only off-note, was in Nic Marks’ rounding-up of the morning. Marks, of the new economics foundation (nef), mistakenly forgot he was at an arts event and not a happiness forum, missing, as he did the cynicism, experience and discontent in the room, (and perhaps wider society).

Whilst many of the people in the session had eloquently described how the arts are, by their very nature political, and I’d opened the session by expressing frustration at societal acceptance of blame for government mismanagement and the crimes of the bankers, Marks focused on what he saw as ‘cheap shots’ at the happiness agenda.1

Now I may be mistaken, but at all the m a n i f e s t o events, I’m mindful of ensuring a couple of things; keeping what I say as consistent as possible, for parity’s sake across the region, and focusing on the long (and rather obvious) history of the arts being more than little baubles and trinkets to pacify people, but as exciting, provocative, subversive and again, political.

By suggesting that cynical politicians may just be hijacking the happiness agenda and arguing our work wasn’t just about making people happy, I apparently blinded Marks to why he was there: to look at the arts in relation to well-being.

And the Five Ways to Well-being by nef are pretty much accepted as good, common-sense ways of looking at day-to-day actions to promote well-being. By connecting with people: being active: taking notice of things beyond our day to day: keeping learning and giving. So no argument there, in fact this ‘latest scientific evidence’ is blindingly obvious.

That’s why we asked Marks to round things off; we thought that all these actions might in fact, contribute towards more fully engaged members of society who connect with others and actively debate and question the status quo: take more than a passing interest in the sound-bites of the popular press and see the potential of shared voices and practice as being part of something bigger: contributing to wider civic society.

Surely then, the result of being a fully engaged citizen might just lead to a more cynical and less superficially ‘happy’ society. Describing my comment about our work not just being about making people happy, as being a ‘cheap-shot’ typical of the media, and for a ‘quick laugh’ Marks risked skewing the whole flavour of the session and devaluing the contributions made.2

I doubt that anyone taking part in the session would question the impact of the arts on well-being, that’s why we’re all involved, we weren’t there to explore the damage we can inflict on each other with our practice.

The point is, that the arts offer so much more than hedonic gratification, and through participation give voice to frustration, anger and cynicism; in other words, art is more than the blind pursuit of happiness (whatever that is) that we’re all told we must aspire to.

Like flat-screen TVs, 4x4 cars or celebrity spray-on tan, it seems happiness is being peddled on the consumerist must-have shopping list. Well, with 2.5 million people unemployed and counting, it looks like the only quick-fire state route to happiness will be through prescription drugs, no doubt on offer through our local National Health Franchise.

Whilst we’re on our way to understanding well-being, (and I’d suggest that the arts and cultural engagement play a big part in that journey), I find it increasingly difficult to imagine how subjective happiness can be identified let alone measured.

And yet as far back as the 2006 Conservative Party Conference, David Cameron has muted the idea of a happiness index, commenting, ‘Let optimism beat pessimism, let sunshine win the day..." Five years later, the NHS, Education and Cultural sectors are undergoing fundamental changes and the banking crisis has thrown the global economy into turmoil. Under the instruction of Cameron, a happiness index is being prepared as I type.

Clive Parkinson
Blue Monday: January 24th 2011

1. In his summing up, Marks said that Cameron and the Government don’t talk about happiness, whereas in reality, there is a wealth of coalition rhetoric on the subject.
2. Rounding off the event and from the lectern, Nic Marks looked me squarely in the eyes and asked, ‘Isn’t happiness the most important thing for our children?’ (Like Ricky Gervais, but without the irony). I wanted to scream, ‘Of course it is, you twerp!’ but I applauded politely thinking, ‘I’d like my children to have a healthy degree of cynicism too; oh and food and shelter, oh and education and love...’

HealthCorrelator for Excel (HCE) is now publicly available for free trial

HealthCorrelator for Excel (HCE) is now publicly available for download and use on a free trial basis. For those users who decide to buy it after trying, licenses are available for individuals and organizations. If you are a gym member, consider asking your gym to buy an organizational site license; this would allow the gym to distribute individual licenses at no cost to you and your colleagues.

HCE is a user-friendly Excel-based software that unveils important associations among health variables at the click of a button. Here are some of its main features:

- Easy to use yet powerful health management software.

- Estimates associations among any number of health variables.

- Automatically orders associations by decreasing absolute strength.

- Graphs relationships between pairs of health variables, for all possible combinations.

The beta testing was successfully completed, with fairly positive results. (Thank you beta testers!) Among beta testers were Mac users. The main request from beta testers was for more illustrative material on how to use HCE for specific purposes, such as losing body fat or managing blood glucose levels. This will be coming in the future in the form of posts and linked material.

To download a free trial version, good for 30 use sessions (which is quite a lot!), please visit the HealthCorrelator.com web site. There you will also find the software’s User Manual and various links to demo YouTube videos. You can also download sample datasets to try the software’s main features.

CoQ10 Adds to Mediterranean Diet’s Anti-Aging Benefits

Elderly men and women who supplement Mediterranean-style meals with coenzyme Q10 (coQ10) enjoy greater antioxidant protection and could slow aging, a Spanish study finds (1).

In a randomized crossover trial, University of Cordoba researchers assigned 20 healthy adults (ages 65 and older) to one of the three dietary protocols for the duration of four weeks: a traditional Western-style diet rich in saturated fats, a Mediterranean-style diet rich in olive oil, or a Mediterranean-style diet supplemented with coQ10 (200 mg/day in capsules).

The scientists found that the combination (Mediterranean-style meals and coQ10) improved antioxidant activity and reduced cellular oxidative stress in the subjects more successfully than the Mediterranean-style or Western-style diet alone.

The Mediterranean-style diet protocols also exhibited greater heart-protective benefits in comparison to the Western-style diet. The scientists noticed a significantly greater decrease in HDL cholesterol (the “good” cholesterol) levels in response to the Western-style meals.

Writing in the December issue of AGE, the authors concluded that the effect of the Mediterranean-style diet rich in olive oil, in combination with coQ10, may have “favorable effects on the aging process” and on the prevalence of age-related conditions.

Previous studies, noted by the authors, have found that the olive-oil rich diet supplemented with coQ10 also improves capillary blood flow and helps maintain healthy blood pressure.

Mediterranean-style diet

A Mediterranean-style diet generally includes greater amounts of fruits, vegetables, whole grains, and olive oil; at least two servings of fish and seafood per week; moderate amounts of poultry, eggs, cheese and yogurt; and fewer meats and sweets.

In this study, the Mediterranean-style diet consisted of 15 percent of calories as protein, 47 percent as carbohydrate, and 38 percent as fat (24 percent monounsaturated fats [from virgin olive oil], 10 percent saturated fat, and 4 percent polyunsaturated fatty acid).

The Western-style diet consisted of 15 percent calories as protein, 47 percent as carbohydrate, and 38 percent as fat (12 percent monounsaturated fats, 22 percent saturated fats, and 4 percent polyunsaturated fats).

Several other studies have pointed to anti-aging benefits from the Mediterranean-style diet. One such study, just published by researchers at Rush University, of Chicago, in the American Journal of Clinical Nutrition linking the diet to a healthier brain in older age (2).

CoQ10 and Oxidative Stress

CoQ10 is a major fat-soluble antioxidant found in all cell membranes, especially within mitochondrial membranes. It’s one of the cell’s most potent scavengers of free radicals, neutralizing the lipid peroxyl radicals that damage cell membranes, proteins and DNA.

Antioxidants are the body’s first line of defense against free radicals and byproducts of metabolism that could lead to cellular decline and dysfunction.

The ability of humans to synthesize coQ10 declines 20 percent for every decade of life after the age of 21. This reduction leads to deficiency, weakness and fatigue throughout the body.

Lower coQ10 levels in tissues and cells can allow for more damage on nearby lipids, proteins and DNA. Because coQ10 is chiefly instrumental (along with selenium) for the regeneration of vitamin E, another potent fat-soluble antioxidant, the diminished coQ10 levels also lead to declines in levels of vitamin E.

Sources:

1. Yubero-Serrano EM, Delgado-Casado N, Delgado-Lista J et al. Postprandial antioxidant effect of the Mediterranean diet supplemented with coenzyme Q(10) in elderly men and women. Age (Dordr ) 2010.
2. Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. Am J Clin Nutr 2010.

Sweet Sugar Alcohols

You’ve probably noticed sugar alcohols before in chewing gum, candies, baked goods, ice cream and diet drinks. These products are also often labeled “sugar free”, “low in calories”, “diabetic-friendly”, and even “tooth-friendly”. Suspicious? We don’t blame you—when you see the words sugar and alcohol together, there’s plenty of reason to start asking questions. However, upon learning a little about these ingredients you’ll find they have unique benefits.

Sugar alcohol sounds worse than it is because chemists create names based on structures—it’s not the type of alcohol that makes you drunk! Sugar alcohols are so named because they are little carbon rings with OH (oxygen-hydrogen) groups on them, also called polyols. These polyols are naturally found in many plants and are easily recognized by the human body (in fact, human cells produce their own sugar alcohols such as sorbitol).

Fewer calories, greater flavor

The truth is that sugar alcohols, when used in correct amounts, can be safe, natural and healthy. They do provide sweetness and energy, but they have fewer calories than sugar (1-3 per gram versus 4 per gram). This results in a low impact on blood sugar and insulin levels, which is why sugar alcohols are often used in products intended for diabetics.

Some sugar alcohols can also be fermented by friendly probiotic bacteria that make up a healthy intestinal flora. A healthy intestinal flora helps support your immune system and can help improve digestion. In addition, sugar alcohols are seldom able to be metabolized by oral bacteria, which is why they’re “tooth-friendly”. They avoid promotion of tooth decay and cavities.

When used in foods, sugar alcohols can be especially useful. They provide bulk and texture that makes foods and candies more enjoyable to consumers. They enhance and deliver a lasting flavor of sweetness as well as provide a “cooling effect”. Particularly in baked goods, they help prevent browning when exposed to heat and also help those foods stay moist over time.

Maltitol

Not all sugar alcohols are the same. There are many with varying attributes. Maltitol, for example, acts in a different way than, say, xylitol. Maltitol is a disaccharide like sucrose (table sugar) and has almost the same level of sweetness and other properties. This makes it very useful for replacing table sugar while offering fewer calories and avoiding promotion of tooth decay.

When consumed, maltitol is broken down by enzymes to glucose and sorbitol. The glucose is easily absorbed, but the sorbitol is resistant to digestion. Because of its resistance to digestion, sorbitol works in similar fashion to prebiotic fiber, fermenting and feeding that helpful intestinal bacteria.

With maltitol, however, there is a concern about overconsumption, especially in people who are unused to sugar alcohols. Consuming an excess of 10g may cause bloating. And, in absence of soluble fiber, consumption of 20g or more can cause loose stool or diarrhea. You’d have the same laxative effect from eating too many fruits like plums, prunes, apples, pears and cherries. These fruits are all high in sorbitol.

Xylitol and Erythritol

What about xylitol and erythritol? These sugar alcohols are not quite as sweet as sugar or maltitol. And they have a stronger cooling effect than any of the other sugar alcohols. You’d recognize their flavor from sugar-free chewing gum. Like maltitol and sorbitol, they offer fewer calories than sugar and don’t promote tooth decay.

Unlike their counterparts, however, xylitol and erythritol are unlikely to ferment and cause bloating or diarrhea. They are considered non-fermentable because intestinal bacteria have difficulty digesting them. After consumption, most erythritol is absorbed easily into the bloodstream, while xylitol is absorbed more slowly.

Xylitol is notable because it’s found to be more effective than other sugar alcohols in reducing cavities. According to recent studies, primarily from Finland, xylitol may not only reduce potential cavities from forming, but even strengthen teeth. Its mechanism is thought to occur by attracting and “starving” cavity-producing bacteria. The Finnish were the first to extract xylitol from birch, but it’s found in many plants, fruits and vegetables, especially berries, plums and raspberries.

Erythritol is naturally found in grapes, melons and mushrooms, as well as in fermented foods like wine, beer and cheese. Because of its ultra-low impact on blood sugar, you’ll also find erythritol often paired with sugars to lessen its blood-sugar effects in foods, with other sugar alcohols, or with natural sweetening herbs such as stevia in natural sweetener packets.

Reference: Brown A. Understanding Food: Principles and Preparation, 3rd ed. Wadsworth, Cengage Learning. 2008.

Brussels sprouts in olive oil

For some fun, I've decided to take pics of some foods I eat and write a bit about them.

For example, these Brussels sprouts in olive oil.

I made a bunch of them for my family and me. They all declined, even my grandma. So I ended up eating them for dinner and for breakfast!

But seriously, they're not only delicious (an acquired taste, I guess), but they're also packed with fiber, carotenoids, vitamins, and minerals.

In addition, like other cruciferous vegetables they do contain some sulfur-rich chemicals that are potentially cancer-protective.

These chemicals are called glucosinolates. When they are chewed they end up as hydrolysis products like indole-3-carbinol.

The breakdown products appear to stimulate the body to eliminate carcinogens more easily and/or by inhibiting cells from becoming cancerous.

They might even induce genomic effects, increasing production of glutathione S-transferases, which metabolize isothiocynates and several other compounds including known carcinogens.

According to epidemiological evidence, eating cruciferous veggies can lower risk of lung, colorectal, prostate, and breadt cancer.

That's why I try to eat cruciferous at least twice a week.

Why the Brussels sprouts? Why not enjoy other cruciferous like broccoli, cabbage, cauliflower, and bok choy?

Mainly, it's because I love the sprouts, especially with olive oil as pictured here. The complexity of its flavor is what I go for really.

But also because they have roughly four times as much glucosinolates than other types of cruciferous veggies.

That's a heavy dose of cancer protection for each sprout!

- Posted using BlogPress from my iPhone

Do you lose muscle if you lift weights after a 24-hour fast? Probably not if you do that regularly

Compensatory adaptation (CA) is an idea that is useful in the understanding of how the body reacts to inputs like dietary intake of macronutrients and exercise. CA is a complex process, because it involves feedback loops, but it leads to adaptations that are fairly general, applying to a large cross-section of the population.

A joke among software developers is that the computer does exactly what you tell it to do, but not necessarily what you want it to do. Similarly, through CA your body responds exactly to the inputs you give it, but not necessarily in the way you would like it to respond. For example, a moderate caloric deficit may lead to slow body fat loss, while a very high caloric deficit may bring body fat loss to a halt.

Strength training seems to lead to various adaptations, which can be understood through the lens provided by CA. One of them is a dramatic increase in the ability of the body to store glycogen, in both liver and muscle. Glycogen is the main fuel used by muscle during anaerobic exercise. Regular strength training causes, over time, glycogen stores to more than double. And about 2.6 the amount of glycogen is also stored as water.

When one looks bigger and becomes stronger as a result of strength training, that is in no small part due to increases in glycogen and water stored. More glycogen stored in muscle leads to more strength, which is essentially a measure of one’s ability to move a certain amount of weight around. More muscle protein is also associated with more strength.

Thinking in terms of CA, the increase in the body’s ability to store glycogen is to be expected, as long as glycogen stores are depleted and replenished on a regular basis. By doing strength training regularly, you are telling your body that you need a lot of glycogen on a regular basis, and the body responds. But if you do not replenish your glycogen stores on a regular basis, you are also sending your body a conflicting message, which is that dietary sources of the substances used to make glycogen are not readily available. Among the substances that are used to make glycogen, the best seems to be the combination of fructose and glucose that one finds in fruits.

Let us assume a 160-lbs untrained person, John, who stored about 100 g of glycogen in his liver, and about 500 g in his muscle cells, before starting a strength training program. Let us assume, conservatively, that after 6 months of training he increased the size of his liver glycogen tank to 150 g. Muscle glycogen storage was also increased, but that is less relevant for the discussion in this post.

Then John fasted for 24 hours before a strength training session, just to see what would happen. While fasting he went about his business, doing light activities, which led to a caloric expenditure of about 100 calories per hour (equivalent to 2400 per day). About 20 percent of that, or 20 calories per hour, came from a combination of blood glucose and ketones. Contrary to popular belief, ketones can always be found in circulation. If only glucose were used, 5 g of glucose per hour would be needed to supply those 20 calories.

During the fast, John’s glucose needs, driven primarily by his brain’s needs, were met by conversion of liver glycogen to blood glucose. His muscle glycogen was pretty much “locked” during the fast; because he was doing only light activities, which rely primarily on fat as fuel. Muscle glycogen is “unlocked” through anaerobic exercise, of which strength training is an instance.

One of the roles of ketones is to spare liver glycogen, delaying the use of muscle protein to make glucose down the road, so the percentage of ketones in circulation in John’s body increased in a way that was inversely proportional to stored liver glycogen. According to this study, after 72 hours fasting about 25 percent of the body’s glucose needs are met by ketones. (This may be an underestimation.)

If we assume a linear increase in ketone concentration, this leads to a 0.69 percent increase in circulating ketones for every 2-hour period. (This is a simplification, as the increase is very likely nonlinear.) So, when we look at John’s liver glycogen tank, it probably went down in a way similar to that depicted on the figure below. The blue bars show liver glycogen at the end of each 2-hour period. The red bars show the approximate amount of glucose consumed during each 2-hour period. Glucose consumed goes down as liver glycogen decreases, because of the increase in blood ketones.

As you can see, after a 24-hour fast, John had about 35 g of glycogen left, which is enough for a few extra hours of fasting. At the 24-hour mark the body had no need to be using muscle protein to generate glucose. Maybe some of that happened, but probably not much if John was relaxed during the fast. (If he was stressed out, stress hormones would have increased blood glucose release significantly.) From the body’s perspective, muscle is “expensive”, whereas body fat is “cheap”. And body fat, converted to free fatty acids, is what is used to produce ketones during a fast.

Blood ketone concentration does not go up dramatically during a 24-hour fast, but it does after a 48-hour fast, when it becomes about 10 times higher. This major increase occurs primarily to spare muscle, including heart muscle. If the increase is much smaller during a 24-hour fast, one can reasonably assume that the body is not going to be using muscle during the fast. It can still rely on liver glycogen, together with a relatively small amount of ketones.

Then John did his strength training, after the 24-hour fast. When he did that, the muscles he used in the exercise session converted locally stored glycogen into lactate. A flood of lactate was secreted into the bloodstream, which was used by his liver to produce glucose and also to replenish liver glycogen a bit. Again, at this stage there was no need for John’s body to use muscle protein to generate glucose.

Counterintuitive as this may sound, the more different muscles John used, the more lactate was made available. If John did 20 sets of isolated bicep curls, for example, his body would not have released enough lactate to meet its glucose needs or replenish liver glycogen. As a result, stress hormones would go up a lot, and his body would send him some alarm signals. One of those signals is a feeling of “pins and needles”, which is sometimes confused with the symptoms of a heart attack.

John worked out various muscle groups for 30 minutes or so, and he did not even feel fatigued. He felt energetic, in part because his blood glucose went up a lot, peaking at 150 mg/dl, to meet muscle needs. This elevated blood glucose was caused by his liver producing blood glucose based on lactate and releasing it into his blood. Muscle glycogen was depleted as a result of that.

Do you lose any muscle if you lift weights after a 24-hour fast?

I don’t think so, if you deplete your glycogen stores by doing strength training on a regular basis, and also replenish them on a regular basis. In fact, your liver glycogen tank will increase in size, and you may find yourself being able to fast for many hours without feeling hungry.

You will feel hungry after the strength training session following the fast though; probably ravenous.

References

Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.

Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.

Bits and Bats…an Arts and Health Networking Miscellany
27th January, 6:00 – 8:00
Venue at MMU: Details will be emailed to you at least 48 hours in advance

Just to remind you that at this networking evening, I’ll be sharing some very quirky films from the early days of the NHS, purely for our fun and conversation. They are wonderful. If you have any film/new media at all that you’d like to share, please let me know in advance.

m a n i f e s t o update…
For those of you who have been involved in these events to date, a big THANK YOU. There’s another event at the Bluecoat Gallery on the 19th.

Its part m a n i f e s t o and part celebration of work underway in Merseyside and if you want to attend, please get in touch with Polly Moseley at pollymoseley@mac.com  

Following the first stage m a n i f e s t o work which has seen a gathering of passion, vision and aspiration of those involved, I’ll be drawing all the strands together for a second stage of activity which will see us coming together and refining what it is, where it goes and what we do with it. By June 2011 we’ll have something very public to share.

The North West Arts and Health Network is past 1500 members…but what does it all mean?

In reality, our reach is potentially far wider than this, as a number of you email this to your networks on my behalf (thank you)!

Remembering that this network is informal and free…what is it that you’d like to see happening? How can we support each other and what would be useful to have online…most anything is possible.

It would be easy for me to put a survey out and ask you all the obvious questions; but what would the point be? Because if I’m asking the questions, I’m steering things just a bit too much.

So what might be a good starting point is if you email me thoughts, ideas and aspirations and I’ll put some of those questions on the BLOG, anonymously, but so others can see the sorts of things people are talking about. So feel free to email me at artsforhealth@mmu.ac.uk and we can beef up our network in ways that are useful to you.


News in from Jeremy Hunt...

… ‘Culture and sport support a range of policy priorities including, but not limited to, economic growth, health and wellbeing, and safer and stronger communities’.

Thanks for that one Jeremy.

See his letter to local authorities below.

29 December 2010

Dear Councillor

We are writing to you about our shared goal of getting better local services for people and to update you on some practical measures to help local authorities delivering cultural and sporting services when the government's overriding priority is deficit reduction, as reflected in the local government finance settlement.

We would like to highlight some of the many examples of improvement and modernisation across local cultural and sporting services. Culture and sport support a range of policy priorities including, but not limited to, economic growth, health and wellbeing, and safer and stronger communities. It is for these reasons that culture and sport are so important to communities and tend to attract significant local interest. Councils across the country have also learned that it is important to prepare for changes with evidence that can be defended.

Through the Future Libraries Programme (FLP) the Local Government Group and Museums, Libraries & Archives Council (MLA) are supporting 36 councils to find new ways to deliver library services without cutting the front line. We thought it would be helpful, ahead of the formal publication of findings from the programme, to share with you examples of the leading savings options that are emerging and our newsletter gives you more information. The MLA and Local Government Group can help if you want to find out more and are available to assist you in looking at a wider range of options and ideas for your library services that could help you save money while minimising the need for cuts to front line services.

Library authorities outside the programme are also developing innovative approaches to providing services:

* Essex County Council will be helping to improve Slough Borough Council's library service and reduce its administration costs from 1 January 2011;
* Investment by Aviva has contributed towards the transformation of York Central Library with more books, the latest technologies and new services;
* In North Yorkshire volunteers at Grassington Hub are at the heart of service delivery.

We are convinced that innovation, led by the energy and experience of councils themselves, is also going to provide the best recipes for modernising cultural services generally in a tougher financial climate.

There are also lots of examples of councils developing different approaches to providing local cultural and sporting services and responding to the economic situation by being innovative:

Many councils are successfully commissioning their cultural services to deliver more efficiently other key service priorities such as adult social care, health, better outcomes for children and young people and economic development;

* Manchester City Council has focused its culture and sport services as major drivers of economic growth, inward investment, and job creation and training;
* Leicester Comedy Festival has developed relationships with communities and the health service to respond to issues such as men's health, teenage pregnancy and healthy eating amongst children and young people;
* Suffolk Artlink manages a series of projects aimed at improving the lives of vulnerable people in Suffolk including older people and their carers;
* In Kirklees a partnership between creative arts organisations offer a range of services for people as part of their mental health and wellbeing care planning services.

There are a number of different ways by which examples such as these are shared widely across the local government sector, including:

LGID's website brings together in one place the learning that is coming out of the "Passion for Excellence" improvement work in partnership with DCMS and key public bodies.

http://www.idea.gov.uk/idk/core/page.do?pageId=21131849

The Living Places website is a suite of online resources developed by DCMS and key public bodies to support the contribution of culture and sport to planning http://living places.org.uk  

LGID has also launched two new publications outlining ways the sector can improve its efficiency through new ways of working and making better use of assets and sources of further help. http://www.idea.gov.uk/idk/core/page.do?pageId=24327034  

Help and advice is available and it could assist you in providing the culture and sport local people will be looking for while making the savings that are needed.

JEREMY HUNT
Secretary of State for Culture, Olympics, Media and Sport

Cllr CHRIS WHITE
Chair, LG Group Culture, Tourism

Vitamin D status affected by obesity

People who are overweight or obese are more likely to have lower circulating levels of vitamin D and may have trouble with conversion to its hormonally active form, a Norwegian study suggests.

These findings, published in the Journal of Nutrition, may partially explain why carrying extra pounds raises risk of several poor health outcomes linked to low vitamin D. The hormonally active form is critical for maintaining cell health, strong bones, a strong immune system, and a healthy heart and brain.

University of Oslo researchers observed almost 1,800 people for six years—about 62 percent obese and 11 percent morbidly obese as indicated by Body Mass Index (BMI)—and found an inverse relationship between higher BMI and serum concentrations of circulating 25(OH)2D and the hormonally active 1,25(OH)2D.

A seasonal variation of both vitamin D metabolites in the obese subjects provided clues that excess weight disturbed the complicated conversion (hydroxylation) of the circulating 25(OH)2D to hormonaly active 1,25(OH)2D in the kidneys.

The authors suggest that measurement of both serum concentrations, 25(OH)2D to 1,25(OH)2D, in overweight and obese persons may be valuable because of “the reduced bioavailability” of the fat-soluble vitamin that “accumulates in excess body fat and muscular tissue.”

The research confirms prior studies’ findings that people who are overweight or obese may need to obtain higher amounts of vitamin D from sun exposure, diet or supplementation. In addition, achieving a healthier BMI is predicted as a way to improve vitamin D status.

Several other factors affect vitamin D status, and include lack of sunlight exposure, skin with higher melanin content (darker skin), older age, low dietary intake, and impaired ability to absorb vitamin D from the diet.

Source: Lagunova Z, Porojnicu AC, Vieth R, Lindberg FA, Hexeberg S and Moan J. Serum 25-Hydroxyvitamin D is a Predictor of Serum 1,25-Dihydroxyvitamin D in Overweight and Obese Patients. J Nutr 2011; 141: 112-117. doi: 10.3945/​jn.109.119495.

My thoughts:

I found this to be an interesting paper. The point is that one of the big reasons for why obesity leads to poor health is because it wrecks your ability to use a powerful hormone, vitamin D. People overweight need more vitamin D to cope, plus will improve vitamin D status when they lose weight. A big deal.

How come evolution hasn’t made us immortal? Death, like sex, helps animal populations avoid extinction

Genes do not evolve, nor do traits that are coded for our genes. We say that they evolve to facilitate discourse, which is alright. Populations evolve. A new genotype appears in a population and then either spreads or disappears. If it spreads, then the population is said to be evolving with respect to that genotype. A genotype may spread to an entire population; in population genetics, this is called “fixation”.

(Human chromosomes capped by telomeres, the white areas at the ends. Telomere shortening is caused by oxidative stress, and seems to be associated with death of cells and organisms. Source: Wikipedia.)

Asexual reproduction is very uncommon among animals. The most accepted theory to explain this is that animal populations live in environments that change very quickly, and thus need a great deal of genetic diversity within them to cope with the change. Otherwise they disappear, and so do their genes. Asexual reproduction leads to dramatically less genetic diversity in populations than sexual reproduction.

Asexual reproduction is similar to cloning. Each new individual looks a lot like its single parent. This does not work well in populations where individuals live relatively long lives. And even 1 year may be too long in this respect. It is just too much time to wait for a possible new mutation that will bring in some genetic diversity. To complicate matters, genetic mutation does not occur very often, and most genetic mutations are neutral with respect to the phenotype (i.e., they don’t code for any trait).

This is not so much of a problem for species whose members reproduce extremely fast; e.g., produce a new generation in less than 1 hour. A fast-reproducing species usually has a short lifespan as well. Accordingly, asexual reproduction is common among short-lived and fast-reproducing unicellular organisms and pathogens that have no cell structure like viruses.

Bacteria and viruses, in particular, form a part of the environment in which animals live that require animal populations to have a large amount of genetic diversity. Animal populations with low genetic diversity are unlikely to be able to cope with the barrage of diseases caused by these fast-mutating parasites.

We make sex chiefly because of the parasites.

And what about death? What does it bring to the table for a population?

Let us look at the other extreme – immortality. Immortality is very problematic in evolutionary terms because a population of immortal individuals would quickly outgrow its resources. That would happen too fast for the population to evolve enough intelligence to be able to use resources beyond those that were locally available.

In this post I assume that immortality is not the same as indestructibility. Here immortality is equated to the absence of aging as we know it. In this sense, immortals can still die by accident or due to disease. They simply do not age. For immortals, susceptibility to disease does not go up with age.

One could argue that a population of immortal individuals who did not reproduce would have done just fine. But that is not correct, because in this case immortality would be akin to cloning, but worse. Genetic diversity would not grow, as no mutations would occur. The fixed population of immortals would be unable to cope with fast-mutating parasites.

There is so much selection pressure against immortality in nature that it is no surprise that animals of very few species live more than 60 years on average. Humans are at the high end of the longevity scale. They are there for a few reasons. One is that our ancestors had offspring that required extra care, which led to an increase in the parents’ longevity. The offspring required extra care chiefly because of their large brains.

That increase in longevity was likely due to genetic mutations that helped our ancestors extend a lifespan that was programmed to be relatively short. Immortality is not a sound strategy for population survival, and thus there are probably many mechanisms through which it is prevented.

Death is evolution’s main ally. Sex is a very good helper. Both increase genetic diversity in populations.

We can use our knowledge of evolution to live better today. The aging clock can be slowed significantly via evolutionarily sound diet and lifestyle changes, essentially because some of our modern diet and lifestyle choices accelerate aging a lot. But diet and lifestyle changes probably will not make people live to 150.

If we want to become immortal, as we understand it in our current human form, ultimately we may want to beat evolution. In this sense, only very intelligent beings can become immortal.

Maybe we can achieve that by changing our genes, or by learning how to transfer our consciousness “software” into robots. In doing so, however, we may become something different; something that is not human and thus doesn’t see things in the same way as a human does. A conscious robot, without the hormones that so heavily influence human behavior, may find that being alive is pointless.

There is another problem. What if the only natural way to achieve some form of immortality is through organic death, but in a way that we don’t understand? This is not a matter of faith or religion. There are many things that we don’t know for sure. This is probably the biggest mystery of all; one that we cannot unravel in our current human state.

Tucson shooting suspect's possible schizophrenia

I am deeply shocked and saddened as I know many of you are by the news of the senseless shooting that happened in Tucson.

As a resident of Chandler, Ariz., I also found that the incident hit a little too close to home; so, admittedly, I was quick (as many others were) to turn to news reports that offered possible reasons for the heinous act -- politics of the day often pointed out as a motive.

After all, Jared Loughner did target a congresswoman and his Web rantings did wreak of politics. Also, Loughner listed several political books among his favorite reads including Mein Kampf, Animal Farm, and The Communist Manifesto.

However, one book not as often mentioned by the media that caught my eye was this one: One Flew Over the Cuckoo's Nest -- this novel, by Ken Kesey, is one I think reveals more about Loughner than the others.

In short, here's the novel's plot: the setting is a mental hospital, and the tale (in a nutshell) is of a "sane" patient, McMurphy, who has a skewed sense that he has entered a world of psychological control, one that he must escape whatever the cost.

After a failed attempt at freedom and the death of his friend, McMurphy finally takes matters into his own hands, and attacks the "Big Nurse" who symbolically represents all the oppression and brainwashing. It's a kind of suicide act, which eventually has him paying the ultimate price when he is given a lobotomy.

I'm reminded of McMurphy when I read Loughner's disconnected comments in a YouTube video he made before the incident about an imagined fear that the government is "implying mind control and brain wash" of the people, controlling their "grammar structure", and tricking them into believing lies about the U.S. flag.

I'm also reminded of schizophrenia. I'm no psychologist, so a thorough diagnosis is obviously warranted, but I've had the experience of having a person close to me be diagnosed with schizophrenia, and witnessed first-hand the irrational fears they have of the world.

So to me, it appears that Loughner exhibits classic signs of this mental disorder, and that he may have a delusion, or an abnormal interpretation of reality, where the U.S. is one big Cuckoo's nest.

Loughner may have acted in what appears to have been politically motivated, but I think we need to think deeper, and it may serve us all to cease from pointing fingers at political rhetoric (although I agree it should be toned down). Let's look at what's really going on here: mental illness. Loughner did something sick, because he is sick.

What should really be part of our conversation today is how we as a society can do a better job at recognizing the signs of mental illness, such as schizophrenia, and how we can best provide care and treatment to those that suffer from it.

Schizophrenia affects around 2.2 million people in the U.S. alone. Proper diagnosis must be performed by a qualified individual, but we should all at least be somewhat aware of what symptoms to look for and here they are from WebMD:

- Social withdrawal
- Depersonalization
- Loss of appetite
- Loss of hygiene
- Delusions
- Hallucinations
- The sense of being controlled by outside forces

At times, schizophrenia can lead sufferers to behave psychotically, become depressed, cause self-harm, make threats of suicide or violence, commit suicide or acts of violence. The risk of violence from a person with schizophrenia is small, but it can become greater with substance abuse.

We need to spread the message: people who think someone they know someone that may have one or more symptoms of schizophrenia, or know someone with the disorder who has discussed suicide or violence, should help them receive medical care immediately.

In ending this post, I'll just say that my thoughts are with U.S. Rep. Gabrielle Giffords -- who I just learned may have a chance at recovery despite a bullet through her brain -- as well as with the thirteen people who were injured, and the families of the six people who died.

Does strength exercise increase nitrogen balance?

This previous post looks at the amounts of protein needed to maintain a nitrogen balance of zero. It builds on data about individuals doing endurance exercise, which increases the estimates a bit. The post also examines the issue of what happens when more protein than is needed in consumed; including by people doing strength exercise.

What that post does not look into is whether strength exercise, performed at the anaerobic range, increases nitrogen balance. If it did, it may lead to a counterintuitive effect: strength exercise, when practiced at a certain level of intensity, might enable individuals in calorie deficit to retain their muscle, and lose primarily body fat. That is, strength exercise might push the body into burning more body fat and less muscle than it would normally do under calorie deficit conditions.

(Strength exercise combined with a small calorie deficit may be one of the best approaches for body fat loss in women. Photo source: complete-strength-training.com)

Under calorie deficit people normally lose both body fat and muscle to meet caloric needs. About 25 percent of lean body mass is lost in sedentary individuals, and 33 percent or more in individuals performing endurance exercise. I suspect that strength exercise has the potential to either bring this percentage down to zero, or to even lead to muscle gain if the calorie deficit is very small. One of the reasons is the data summarized on this post.

Two other reasons are related to what happens with children, and the variation in spontaneous hunger up-regulation in response to various types of exercise. The first reason can be summarized as this: it is very rare for children to be in negative nitrogen balance (Brooks et al., 2005); even when they are under some, not extreme, calorie deficit. It is rare for children to be in negative nitrogen balance even when their daily consumption of protein is below 0.5 g per kg of body weight.

This suggests that, when children are in calorie deficit, they tend to hold on to protein stores (which are critical for growth), and shift their energy consumption to fat more easily than adults. The reason is that developmental growth powerfully stimulates protein synthesis. This leads to a hormonal mix that causes the body to be in anabolic state, even when other forces (e.g., calorie deficit, low protein intake) are pushing it into a catabolic state. In a sense, the tissues of children are always hungry for their building blocks, and they do not let go of them very easily.

The second reason is an interesting variation in the patterns of spontaneous hunger up-regulation in various athletes. The increase in hunger is generally lower for strength than endurance activities. The spontaneous increase for bodybuilders is among the lowest. Since being in a catabolic state tends to have a strong effect on hunger, increasing it significantly, these patterns suggest that strength exercise may actually contribute to placing one in an anabolic state. The duration of this effect is approximately 48 h. Some increase in hunger is expected, because of the increased calorie expenditure during and after strength exercise, but that is counterbalanced somewhat by the start of an anabolic state.

What is going on, and what does this mean for you?

One way to understand what is happening here is to think in terms of compensatory adaptation. Strength exercise, if done properly, tells the body that it needs more muscle protein. Calorie deficit, as long as it is short-term, tells the body that food supply is limited. The body’s short-term response is to keep muscle as much as possible, and use body fat to the largest extent possible to supply the body’s energy needs.

If the right stimuli are supplied in a cyclical manner, no long-term adaptations (e.g., lowered metabolism) will be “perceived” as necessary by the body. Let us consider a 2-day cycle where one does strength exercise on the first day, and rests on the second. A surplus of protein and calories on the first day would lead to both muscle and body fat gain. A deficit on the second day would lead to body fat loss, but not to muscle loss, as long as the deficit is not too extreme. Since only body fat is being lost, more is lost on the second day than on the first.

In this way, one can gain muscle and lose body fat at the same time, which is what seems to have happened with the participants of the Ballor et al. (1996) study. Or, one can keep muscle (not gaining any) and lose more body fat, with a slightly higher calorie deficit. If the calorie deficit is too high, one will enter negative nitrogen balance and lose both muscle and body fat, as often happens with natural bodybuilders in the pre-tournament “cutting” phase.

In a sense, the increase in protein synthesis stimulated by strength exercise is analogous to, although much less strong than, the increase in protein synthesis stimulated by the growth process in children.

References

Ballor, D.L., Harvey-Berino, J.R., Ades, P.A., Cryan, J., & Calles-Escandon, J. (1996). Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss. Metabolism, 45(2), 179-183.

Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.

Annus horribilis?

Mark Wallinger

A Plea for Pessimism...

Last November I had the pleasure of speaking at the 2nd Annual International Arts and Health Conference in Melbourne. My paper; A Brightly Coloured Bell-Jar explored the relationship between our aspiration to well-being and increased dependency on medication for all our ills. You can hear a podcast of this paper at http://www.artsforhealth.org/podcasts and it will be available in print in February 2011.

Polly Morgan

Two pieces of writing that echo and expand on some of the themes I raised are below.

Is this the end of the children’s decade?

Polly Toynbee questions whether voters believe David Cameron's new year's message, that: "We're tackling the deficit because we have to – not out of some ideological zeal. This is a government led by people with a practical desire to sort out this country's problems, not by ideology. When we talk of building a bigger, stronger society, we mean it." Or will they believe Ed Miliband's view that the "irresponsible pace and scale" of the cuts is a "political choice by those in power, not necessity"?

http://www.guardian.co.uk/commentisfree/2010/dec/31/end-childrens-decade-coalition 

Steve Bell; The Guardian

How to Stop Living and Start Worrying.

Since when did happiness, wisdom and contentment become the cornerstones of a fulfilling life? Whatever happened to doubt? Instability? Melancholia? 

This month, Polity Press are releasing How to Stop Living and Start Worrying, a collection of interviews with Simon Critchley, which playfully parodies the conventional self-help manual. Critchley sketches an alternative view of the role philosophy plays in our lives today, covering an ambitious range of topics: from science and religion, to poetry and politics, love and humour, life and death.

http://www.apieceofmonologue.com/2010/09/critchley-stop-living-start-worrying.html

…and finally

The next  M A N I F E S T O  event will be on the 19^th January at the Bluecoat Gallery in Liverpool…details to follow.

...and don’t forget the first North West Arts and Health Networking session of the year on January 27^th between 6:00 and 8:00 in the evening when I’ll be sharing some odd little films from the birth of the NHS in the 1940’s and I encourage you to submit material for sharing too. I’ll confirm the venue the week before, but for now, could you RSVP to artsforhealth@mmu.ac.uk