GLuten-Free Blueberry Corn Muffins

Summery, fresh blueberry corn muffins- gluten-free.

August is fast approaching. I am trying not to think about it. I am baking blueberry corn muffins. Denial ain't just a river in Egypt. Or so I'm told. I am constructing my best defense to put off thinking about hauling our ocean-loving selves back to the dusty stoic hills of Ojo Caliente- 913 miles away from my sons, 915 miles from the sea.

Anyone out there want to buy a charming casita with mesa sunset views? Two kiva fireplaces. Saltillo tile floors. Vigas. All the rustic Southwest vibe you could ask for. Price reduced (thrice). To less than what we paid for it.

I don't pretend to understand the bigger picture, the honking beast of our lumbering economy. I'm no good at math- even when the economy is not melting down, humming along to its own sweet tune, nevermind comprehending the intricate ins and outs and ups and downs of depression economics and the breathtaking depths of Wall Street greed and extra sensitive interest rates that pout and pose and tease like strippers sending brokers into sweating Xanax popping frenzy. Not to mention, I cannot wrap my poetic visual brain around those epic taxpayer funded Wall Street buy-outs.

I'm an artist. I have always lived by the seat of my pants, without health insurance, without an IRA. I don't live by a plan. I live by intuition. Inspiration. I play with paint (not a skill valued by many people in our big screen spectacle loving culture). So I probably shouldn't have become a home owner. It was probably my fault. I should have known better. I've learned my lesson. I'm letting go. I'm saying no to mortgages. For now.

And I'm baking muffins.

I'm trying to practice my best Zen-Lebowski detachment (the waves help). And yeah. We still have three weeks. Miracles happen.

As always?

I'm hoping for the best.

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Canto and Owen [Rhesus Monkeys]

The industry worth billions of dollars every year is the cosmetic industry, holding back those wrinles, everyone trying to stay young. What is one of the most important ways of looking younger for longer? > Calorie Restriction < Contrary to earlier reports that fatter humans look younger than their thinner people, remaining slim from a young age and staying this way is likely to keep away the white hair and wrinkles. This has been shown with mice, monkeys and dogs that have been put on CR. The CR group always look youger. Below are some high resolution pictures of two rhesus monkeys around the same age, owen is just over 1 year older than canto. Canto is 27 years of age right now and looks like a youthful rhesus monkey at half his age (and by the way, 27 in human years would be 81 human years!!!). This is achieved by a reduction in calories alone. I could only specualte that with sun avoidance, applying some basic skin care routine, and various polyphenols found in foods we regularly consume on a CR diet, and not frowning a lot and creasing of your forehead. I naturally avoid this and don't hardly ever crease my forehead, also I try to avoid squinting. Wearing a cap helps, sun glasses probably better for this.

I expect for the younger people who start CR before much of the apparent aging skin has already occured could go on to look extremely youthful in middle age.

Twice last week I got asked my age, I joined library, and I also got asked by a nurse how old I was. Both thought I was around 16-17 years old, and I'm 3 months away from being 25! Is it the CR? :D I guess the difference can only grow over time. Is it possible to look only 25 at 50 years of age??? Maybe that might be pushing it, but it will be an interesting thing to see hehe.


ZOOM INTO PICTURES FOR BETTER DETAIL

NORMAL DIET

CALORIE RESTRICTION DIET

The Diet-Heart Hypothesis: Subdividing Lipoproteins

Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk.

Lipoproteins Can be Subdivided into Several Subcategories

In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):

The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease.

Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder.

Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).

Diet Affects LDL Subcategories

The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):

Out of the 87 men with pattern A on the high-fat diet, 36 converted to pattern B on the low-fat diet... Taken together, these results indicate that in the majority of men, the reduction in LDL cholesterol seen on a low-fat, high-carbohydrate diet is mainly because of a shift from larger, more cholesterol-enriched LDL to smaller, cholesterol-depleted LDL [sdLDL].

In other words, in the majority of people, high-carbohydrate diets lower LDL cholesterol not by decreasing LDL particle count (which might be good), but by decreasing LDL size and increasing sdLDL (probably not good). This has been shown repeatedly, including with a 10% fat diet and in children. However, in people who already exhibit pattern B, reducing fat does reduce LDL particle number. Keep in mind that the majority of carbohydrate in modern America comes from refined wheat and sugar; a diet of unrefined carbohydrate may not have these effects.

Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:

In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid [as well as palmitic acid], was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate [density] were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL.

Participants who ate the most saturated fat had the largest LDL, and vice versa. Kudos to Dr. Krauss for publishing these provocative data. It's not an isolated finding. He noted in 1994 that:

Cross-sectional population analyses have suggested an association between reduced LDL particle size and relatively reduced dietary animal-fat intake, and increased consumption of carbohydrates.

Diet Affects HDL Subcategories

Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:

The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.

Saturated and omega-3 fats selectively increase large HDL. Dr. B. G. of Animal Pharm has written about this a number of times.

Wrapping it Up

Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are refined wheat and sugar.  Healthier sources of carbohydrate have different effects on blood lipids.
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.

Vegetarian Puttanesca for Two

Easy pasta putanesca- gluten-free with rice spaghetti.

Oh, you paint, too? is the faint, flat interest we get, we artist's wives who paint. Inevitably followed by, Isn't that difficult? In fact, I assure them, it couldn't be easier. (Try being married to a real estate agent who sprays Sun-In in his hair, I want to say, but don't.)

The scene is my husband's art opening and I play my role with decorum, clutching my plastic cup of Australian Chardonnay.

Do you compete? Darling, this question says a lot more about you than than me. No, I always answer, trying not to audibly sigh. We mutually admire. Then comes the big one. The favorite question.

Does he influence your work? (The subtext being, of course, he is the man, after all.)

I influence his, I answer, slugging down the last warm drop of wine. They will smile their awkward smile at this and wobble toward the grapes and brie. The word tedious comes to mind.

I catch my husband looking at me through the peanut nibbling crowd. He raises an ironic eyebrow. I laugh. A sparkled perfumed woman leans in to him for a kiss on the cheek. He is polite. I will tell him later he smells like Bloomingdale’s.

At home he will make me an ice cold vodka martini. We will kick off our shoes and eat spaghetti to Chet Baker. So what's on your agenda for tomorrow? he will ask. Maybe painting, I will say with a yawn. Or blogging. I'm not just an Artist's Wife, you know. 

Nope, he always says. You're the cutest girl ever.

Yeah, I remind him, You're lucky I'm a new-school feminist.

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MRFIT Mortality

The Multiple Risk Factor Intervention trial was a very large controlled diet trial conducted in the 1980s. It involved an initial phase in which investigators screened over 350,000 men age 35-57 for cardiovascular risk factors including total blood cholesterol. 12,866 participants with major cardiovascular risk factors were selected for the diet intervention trial, while the rest were followed for six years. I discussed the intervention trial here.

During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):


Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.

Possible explanations from other studies include higher infection rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.

The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.

The Diet-Heart Hypothesis: A Little Perspective

Now that we've discussed the first half of the diet-heart hypothesis, that saturated fat elevated total and LDL cholesterol, let's take a look at the second half. This is the idea that elevated serum cholesterol causes cardiovascular disease, also called the "lipid hypothesis".

Heart Attack Mortality vs. Total Mortality

We've been warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups: If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group.

Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.): Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population.

These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.

The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). This suggests that total blood cholesterol as a marker of heart attack risk is not universal. It would not necessarily apply to someone eating a non-Western diet.

Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value

So far, this probably hasn't shocked anyone. Most people agree that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets (lipoproteins) containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.

The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.

The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is substantially higher than someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this observation in a future post.

In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins).

Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is some combination of high LDL (particularly LDL particle number), low HDL, and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.

Quinoa Salad with Yellow Tomatoes, Kalamata Olives, Basil + Mint

A light and easy quinoa salad recipe with mint.

I've written about quinoa more than once, so I doubt, Dear Reader, you need me to list all the pro-quinoa reasons why you should try this gluten-free faux grain. You already know it's high in protein. You know how easy it is to cook. You are well aware that quinoa works as a salad- warm or cold- or as stuffing for big juicy mushrooms or rather unconventional stuffed cabbage rolls that might cause your Bubbe to sit up straight in her chair and say, Oy, have I never heard of such a thing! Where do you get these ideas, Shayna Punim?

So I'm not going to wax all educational on ya.

I'd rather wax philosophical. I haven't felt practical. Or pragmatic. Truth is, I sold off furniture to be here. To get out. It's been a long, dry three years in the desert, and living here in Santa Monica is like living inside an intricate dream. The edges here are soft. The colors are gauzy with the salt air. We walk the winding path in Palisades Park at dusk and pass by strangers who meet our eyes and smile- ever so slightly.

As if we share a secret.

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The Diet-Heart Hypothesis: Stuck at the Starting Gate?

The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack.

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because the evidence that typical dietary amounts cause heart disease in humans is weak.  Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the main source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 eggs per week (click for larger image): The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not have a large impact on serum cholesterol in the long term, perhaps because humans are adapted to eating cholesterol. Most people are able to adjust their own cholesterol metabolism to compensate when the amount in the diet increases. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology.

The first half of the diet-heart hypothesis states that eating saturated fat raises blood cholesterol. This has been accepted without much challenge by diet-health authorities for nearly half a century. In 1957, Dr. Ancel Keys proposed a formula (Lancet 2:1959. 1957) to predict changes in total cholesterol based on the amount of saturated and polyunsaturated fat in the diet. This formula, based primarily on short-term trials from the 1950s, stated that saturated fat is the primary dietary influence on blood cholesterol.

According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were significant flaws in the data from the very beginning, which were pointed out in this critical 1973 literature review in the American Journal of Clinical Nutrition (free full text).

The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect sometimes had more to do with LA lowering blood cholesterol than saturated fat raising it. This is not at all what I was expecting to find when I began looking through these trials.

Reading through the short-term controlled trials, I was surprised by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and non-optimal study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and consistently demonstrable.  

The long-term data are not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA certainly does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).  The small changes that did occur could have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions.

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Disease by Dr. Harumi Okuyama et al.): What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). 

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not the case. The Masai traditionally get a high proportion of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating practically nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man? Junk food.

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s).  Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Does dietary saturated fat influence total cholesterol and LDL over the long term?  I don't have the answers, but I do think it's interesting that the evidence is much less consistent than it's made out to be.  It may be that if dietary saturated fat influences total cholesterol or LDL concentration in the long term, the effect is is secondary to other factors.  That being said, it's clear that linoleic acid, in large amount, reduces circulating total cholesterol and LDL.

Comments on the Rhesus Monkey study

CALORIE RESTRICTION REALLY DOES WORK IN MONKEYS

Over the past few days I've been looking around on the internet, checking out the CR Society email lists and the talk among the life extension community to see what others think of the study and whether or not this does really support calorie restriction working in non human primates and possibly humans. First lets look at the survival curve for overall mortality and non age related mortality. First if you haven't read the first post I did on this, scroll down to check it out first.

As you can see there is a big difference in survival in survival curve which excludes deaths from certain causes that are thought not to be caused by diseases and aging. Seven of the control Monkeys and Nine CR Monkeys died of non–age-related causes, which included complications of anesthesia, gastric bloat, endometriosis, and injury.

Anesthesia - The monkeys every year go through a cycle of tests, in order to perform some of these the monkeys have to be sedated. Sometimes even if the monkey was otherwise healthy, things can go wrong. The question is what has this got to do with aging, and should it be included when looking at the life extending effect of Calorie Restriction. Since the monkeys I believe are put under anesthesia quite frequently, possibly at least once a year (although I need to check on this to make sure) then there can be a risk when doing this. But if a monkey dies from anesthesia it tells us absolutely nothing about whether the animals aging was being slowed down or not by calorie restriction. Most humans do not go under anesthesia once or twice a year to have extensive medical tests done on them, in humans more care is probably taken as well in order not to kill the patient. If however there was a trend that as the monkeys aged they were more suceptible to death from anesthesia then I could understand including it in the age related mortality survival. Also taking into account any chronic diseases the subject might have had prior to going under anesthesia. The fact is these deaths could have been very well preventable. The researchers also never noted any increased risk of anesthesia deaths for the calorie restricted monkeys.

Injury - Accidents cannot be totally prevented. If someone fell and suffered severe head trauma, does this again tell you anything about whether or not calorie restriction has slowed down (or not) aging? Clearly the answer is no. One can possibly argue that the rhesus monkey might have been weak from aging and fell. But we don't know the details of how the injury occured, so we can only speculate. However the fact is accidents happen to 'anyone' and they do not tell you anything about aging other than when we see increase risk of falls from elderly humans which result in hip fracture and death. Should injuries be exlcuded? Absolutely! I have yet to see a good argument why they shouldn't.

Gastric bloat - I do not know how many monkey died from this but again this is a totally preventable death! From an article published in 2002 in the Wall Street Journal when refering the survival of the monkeys;

"Those figures exlcude monkeys whose deaths wree deemed accidental, such as when a batch of overcooked food caused a fatal stomach ailment called gastric bloat"

This is something that can happen at absolutely any age and should have been prevented, there is no reason at all to include it in the survival curve, and once again does not show whether or not CR was working. It was simply a preventable accident that can happen to any healthy monkey, both CR'd and Ad lib.

These are all deaths which I am very comfortable with the researchers excluding from their survival stats. They really do not tell us anything about aging and can happen at any age, and they were not increasing in frequency with age. In fact quite a few of the deaths seemed to be in the early stages of the study and later on the carers were better able to prevent more deaths from the causes above. In time I suspect that the overall mortality curve will show statistical significance. As there are three groups in the study we cannot tell what the average lifespan of the calorie restricted and ad lib groups are, but this data should be in quite soon. All animals are now apparently 27 years of age which is about the lifespan for a rhesus monkey, with the maximum being 40 years. So we could be waiting quite a while yet if a few of the monkeys reach 40 and beyond. So far almost all of the control monkeys have age related conditions that could eventually result in death, whereas in the CR animals a large percentage of them are in good health. As you can see below, througout the course of the study the control animals are experiencing more cancer, more cardiovascular disease, and big problems regulating glucose. Monkeys are particularly suceptible to age related diabetes than humans are, but calorie restriction seems to completely prevent this and even in two of the rhesus monkeys it reversed pre diabetes stage when they entered the study.

This tells us one important thing that all of us wish to have, a good quality of life. When on CR we are likely to spend more years with good health and then less time with ill health before death. It's not uncommon that people today spend decades with chronic health conditions that could be almost completely preventable. There has been some commentary about this study on the CR lists, this was one interesting point.

Michael Rae says; "This is the best of the 3 nonhuman primate studies, and still has some flaws: the actual differnce in Calorie intake has dwindled down to almost zero, because none of the animals are very engaged with their rather monotonous and restricted lives; the food isn't the best; there were definitely nutritional problems (such as excessive retinol, early on) in the diets; we don't *really* know how how to best care for and feed nonhuman primates, nor how long they can live in captivity, because so few have been studied; and above all, there's evidence that the AL group probably should've been restricted a bit more and the CRed animals restricted even further in turn (no effects on menstruation in the females, and probably some of the AL diabetes is related to modest overweight)."

Researchers are usually careful to make sure that the control group are normal weight and not affected by issues largely releated to being overweight. So animals are usually restricted by 20% from their true ad lib intake to avoid these complications. Michael is saying that the both groups should have been restricted more. I do believe the researchers found problems with restricting calories more severily in the CR group, they were deemed to be too thin and possibly pose future health problems which might cause issues further on in the study. I think the researchers were right to er on the side of caution here because the last thing we want is a complete failure because of health complications. There might have been none and most of the monkeys apparently were fine but like other studies in dogs, they increased the calories of some of the rhesus monkeys. I'm unsure if the information about there not being a difference between the both groups in terms of calorie intake, I heard this was an issue at the NIH study but not wisconsin. Maybe Michael has communicated with the researchers at Wisconsin or other people who knows about the situation there. And finally the food the monkeys are given, they are given monkey chow which is not the best food but it would be extremely difficult to give them anything else. With humans we can control our own diets, it's quite easy, and we know more in terms of what we need to stay healthy.

If anything the humans will respond even better. We have good access to health care (although the monkeys did recieve good health care also), we are not stuck in cages all our lives which would surely leave all of us quite depressed. The human data is pretty strong, even taken at face value and not comparing to the control groups, it's still very impressive. Almost every marker of health is improved by CR. Maybe now people should stop using the saying "It doesn't make you live longer, it just seems like it". Because this is not true :-)

Calorie Restriction is still the best way we can extend our lives, it's the best way to reach 100 and beyond, and it's the best way to ensure that you reach the point when medicine has advanced enough to slow and reverse aging.

If anyone has any good objections and why they should include the deaths I mention above, I'd love to hear it. So far there has been no good reasons why they have any indication or not whether CR is working.

EDITED: 13:30 15/07/2009 --

IN RESPONSE TO JUNK FOOD SCIENCE BLOG

Responding to some things from JunkFoodScience where I seen that there were many mistakes and misleading words.


Sandy Szwarc says;

"The non-aging-related causes of death included monkeys who died while taking blood samples under anesthesia, from injuries or from infections, such as gastritis and endometriosis."

The monkeys did not die from infections or gastritis. They mostly died for prentable causes and more care should have been taken i.e Not overcooking batch of food and killing the monkeys with gastric bloat. Anesthesia and injuries I already explained.

Sandy Szwarc says;

"As the supplemental data explains, 16 deaths from “non-age-associated causes were censored and their age of death used as the time variable in the regression"

She words it so the average reader without looking more into it would probably assume these 16 deaths or much more of them were all from the CR group. When is was 9 deaths for CR and 7 for ad lib.

Sandy Szwarc says

"but they could realistically be adverse effects of prolonged calorie restrictions on the animals’ health, their immune system, ability to handle stress, physical agility, cognition or behavior."

Well no there is no data that supports immune systems were weakened in monkeys and actually there is evidence monkeys have better immune systems under CR. They never died from infections in the study. The CR animals usually are able to withstand greater stress as seen in other lab animals, the CR monkeys were reported to be in better shape physically, as you can see by their posture and the way they move on videos. And in terms of cognition, it seems the CR monkeys are doing better from an earlier paper which showed better cognitive skills and problem solving. Not much behaviour differences were noted in the papers on the primates.

Then she makes this claim

"the control animals were overfed 20% more than their usual diet, while the CR monkeys’ diets were adjusted to keep them about 30% less than the control monkeys."

The control group were not as I recall fed 20% more than their ad lib intake, and they also had their food taken away from them also after the period of feeding time was over. She doesn't supply any references to support what shes saying. Then she assumes that the CR monkeys were fed 10% less to achieve a 30% reduction [after the 20% increase in control group] in calories? No, each CR monkey had its baseline intake calculated and reduced by 10% each month until reaching 30% below its normal calorie intake. The ad lib calorie intake was not increased by 20% to achieve this 30% reduction. The Ad lib monkeys were not true eat your brains out ad lib group, this was done at a previous study in Maryland where the control grop only reached 25 and CR group 32, but the ad lib intake in this study was also somewhat restricted to prevent obesity. Although it might have needed to be restricted a bit more and the CR group more also. All animals have a feeding period of about 8 hours, and food is removed from both groups and counted. So two differences in the Rhesus monkey studies. The NIA study reduced calorie intake from tables of how much each monkey should each should eat for their age and body weight, and the Wisconsin study reduced CR animals by 30% from their baseline intake after recording it for 3 - 6 months before starting the 10% reduction in calories every month for 3 months until reaching 30% restriction.

This presentation about the study shows that the female restricted group are now around 20% restricted comapred to the control group, whereas by their own baseline intake they at are 30% fewer calories. The males are able to stay around 30% restriction over time. This is the food intake for CR and Control group, they have their food measured everyday.



Some final thoughts

Now a suggestion to everyone. When reading blogs around the internet please try to be aware of false information, do a bit of research into it yourself. Many people have their own agenda usually don't actually read into the science properly, and they try to use clever words and twist stories around. Sometimes the mistake is genuine, but bottom line is look into yourself if you're not convinced. As for the JunkFoodScience blog, there were many obvious mistakes even after my first quick read through. Unfortunately for the average person reading they might easily be persuaded by people like her. My job here is to try and give you the latest information and media on CR, trying to be as honest as I can, and report the latest studies on health and try to give the correct data and not 'twist' stories around.

Thanks to a comment I recieved earlier you can read about Ms. Szwarc HERE . From looking at her funding sources, like McDonalds, she isn't exactly the kind of person you wan to listen to. She defends obesity, junk food, she claims obesity makes you healthier and a bunch of other crap. She is quite a good writer and can easily convince some people, don't be one of them. Also check another post about Szware HERE .

Egg-Free Olive Oil Mayo

How to make an egg-free olive oil mayo.

One truth about myself that I'm learning- more and more- is it's the little things in life that stick.

It's the small moments I remember instead of the big ones, the quiet tender gesture rather than grandiose theatrics designed to make you swoon. Big and blown out- for me- simply fizzles and dissipates. There are gaps in my memory that reveal this proclivity to live off to the side, observing the small and overlooked, wondering what all the mainstream fuss is about. So much of what parades by as important strikes me as a lot of loud and self conscious whistling in the dark.

I prefer and savor the simple pleasures in life. Hot water and soap. Holding hands. Opening a new book. The unlauded bite of a new recipe that works- especially if you missed a certain taste- a condiment taken for granted, a spoonful most Americans plop onto their turkey sandwich, or stir into crab cakes, potato or tuna salad with no more thought or effort than simply reaching into the fridge and opening a jar.

Yes, I'm talking about mayo.

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Whats going on the garden

Just a small garden update.

Broccoli plants - I had to pull two of the plants, the rest have held up well and the broccoli are growing well, albiet a small issue in one of the boxes which might be a boron deficiency. Though still perfectly edible broccoli. Here is the one I just harvested about 10 minutes ago. It came to around 450g but on here the scale must of went off.



Spinach - Well it all bolted and I pulled it up, I will put spinach back in after the fall and also MANY more carrots that I'm just about to sow tomorrow. Next time I defienitely need to start protecting my spianch better.

Cherry Tomatoes - I have totally lost count how many are growing, there are just so many flowers everywhere on the plants, all which will turn into lush small cherry tomatoes. I'm waiting for quite a lot to ripen at the moment but the plants are doing really well and producing a hell of a lot. Can't wait to harvest them, I'm gonna net them in the week too so I can stop them being eaten as they riepn. I must have hundreds growing at the moment. One mistake, I haven't really pruned the plants, I think I'm going to start that now. There is only one tomato plant that is not doing much, and that was the one which I put in the pot. I have now transplanted it into the big garden box.


Carrots - I pulled up a few carrots the other day and they were still a bit smaller than I expected, so I'll be leaving them for another 3 weeks. Though I ate what I harvetsed and they were nice. I just used them in a small salad I had.

Quinoa Muffins with Pecans

High protein quinoa flakes make this gluten-free muffin yum.

Not since my Quinoa Breakfast Cake recipe have I enjoyed a morning treat more. I am seriously digging these cute little quinoa beauties. I started out imagining a quinoa breakfast bar, an easy to-go treat that might fuel my morning walks on the beach (I've been walking three miles almost every day- which is a minor miracle, for those of you who remember the trippy Richard Gere incident). I wrote up a recipe I thought might create a higher protein snacking bar I could munch with my mug of Irish Breakfast Tea as I browse, bleary-eyed and yawning through the morning chirps over at Twitter.

But it became apparent rather quickly this batter was born to be muffins. I could just tell. It had that perfect stretchy je ne sais quoi that I knew deep down in my private tiny girl heart would urge the dark chocolate studded dollops of earthy quinoa goodness to rise into tender golden domes like champs.

So I followed my intuition and switched gears and veered into Muffin Land.

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The Finnish Mental Hospital Trial

This diet trial was conducted between 1959 and 1971 in two psychiatric hospitals near Helsinki, Finland. One hospital served typical fare, including full-fat milk and butter, while the other served "filled milk", margarine and polyunsaturated vegetable oils. Filled milk has had its fat removed and replaced by an emulsion of vegetable oil. As a result, the diet of the patients in the latter hospital was low in saturated fat and cholesterol, and high in polyunsaturated fat compared to the former hospital. At the end of six years, the hospitals switched diets. This is known as a "crossover" design.

The results were originally published in 1972 in the Lancet (ref), and a subset of the data were re-published in 1979 in the International Journal of Epidemiology (ref). They found that during the periods that patients were eating the diet low in saturated fat and cholesterol, and high in vegetable oil, male participants (but not females) had roughly half the incidence of heart attack deaths. There were no significant differences in total mortality in either men or women. The female data were omitted in the 1979 report.

This study is often cited as support for the idea that saturated fat increases the risk of heart attack. The reason it's cited so often is it's one of a minority of trials that came to that conclusion. The only other controlled trial I'm aware of that replaced animal fat with polyunsaturated vegetable oil (without changing other variables at the same time) and found a statistically significant decrease in cardiovascular deaths was the Los Angeles Veterans' Administration study. However, there was no difference in total mortality, and there were significantly more heavy smokers in the control group. The difference in heart attack deaths in the V.A. trial was 18%, far less than the difference seen in the Finnish trial.

I can cite three controlled trials that came to the opposite conclusion, that switching saturated fat for vegetable oil increases cardiovascular mortality and/or total mortality: the Anti-Coronary Club Trial (4 years), the Rose et al. corn oil trial (2 years), and the Sydney Diet-Heart trial (5 years). Other controlled trials found no difference in total mortality or heart attack mortality from this intervention, including the National Diet-Heart Study (2 years) and the Medical Research Council study (7 years). Thus, the Finnish trial is an outlier whose findings have never been replicated by better-conducted trials.

I have three main bones to pick with the Finnish trial. The first two are pretty bad, but the third is simply fatal to its use as support for the idea that saturated fat contributes to cardiovascular risk:

1) A "crossover" study design is not an appropriate way to study a disease with a long incubation period. How do you know that the heart attacks you're observing came from the present diet and not the one the patients were eating for the six years before that? The Finnish trial was the only trial of its nature ever to use a crossover design.

2) The study wasn't blinded. When one wants to eliminate bias in diagnosis for these types of studies, one designs the study so that the physician doesn't know which group the patients came from. That way he can't influence the results, consciously or unconsciously. Obviously there was no way to blind the physicians in this study, because they knew what the patients in each hospital were eating. I think it's interesting that the only outcome not susceptible to diagnostic bias, total mortality, showed no significant changes in either men or women.

3) The Finnish Mental Hospital trial was not actually a controlled trial. In an editorial in the November 1972 issue of the Lancet, Drs. John Rivers and John Yudkin pointed out, among other things, that the amount of sugar varied by almost 50% between diet periods. In the December 30th issue, the lead author of the study responded:

In view of the design of the experiment the variations in sugar intake were, of course, regrettable. They were due to the fact that, aside from the fatty-acid composition and the cholesterol content of the diets, the hospitals, for practical reasons, had to be granted certain freedom in dietary matters.

In other words, the diets of the two hospitals differed significantly in ways other than their fat composition. Sugar was one difference. Carbohydrate intake varied by as much as 17% and total fat intake by as much as 26% between diet periods (on average, carbohydrate was lower and total fat was higher in the polyunsaturated fat group). The use of psychiatric drugs with known cardiovascular side effects differed substantially between groups and could have accounted for some of the difference in cardiovascular events.  

The definition of a controlled trial is an experiment in which all variables are kept reasonably constant except the one being evaluated. Therefore, the Finnish trial cannot rightfully be called a controlled trial. The fact that the result has never been replicated casts further doubt on the study.
I could continue listing other problems with the study, such as the fact that the hospital population included in the analysis had a high turnover rate (variable, but as high as 40%), and patients were included in the analysis even if they were at the hospital for as little as 50% of the time between first admission and final discharge (i.e., they came and went). But what's the use in beating a dead horse?

Calorie Restriction Extends Lifespan in Monkeys

CALORIE RESTRICTION WORKS IN MONKEYS

Just before I left for work earlier today I had a google alert that read something like "Calorie Restriction extends lifespan in Primates". Well not much of a surprise, but happy to read the paper when I can. The article I first looked at was from wired.com. Here is what they said;

"Up until now, all the clear-cut evidence that caloric restriction slows aging has come from lower organisms,” said John Holloszy, a Washington University gerontologist who studies caloric restriction in people and was not involved in the current monkey study. “This is the first study to show that caloric restriction slows aging in a primate species. And of course, we’re primates, too. It’s a lot more relevant to humans than the mouse.”

Click image to enlarge (best quality pic of Canto and Owen)

"All the surviving monkeys are now at least 27 years old, the rhesus equivalent of old age. Those fed a calorically restricted diet have dramatically lower levels of cancer, diabetes, heart disease, brain atrophy and lean muscle loss. Just five of the 38 restricted monkeys have died from age-related causes, compared to 14 of 38 in the control group."

Click image to enlarge

The CR monkeys seem to be looking youger and also keeping a nice fur coat as is quite clear in this picture

Does this make you more confident that CR will work in humans? For me the answer is yes. They visually looking younger, they're also showing big differences in survival.

Source; WIRED

Unrefined vs. Refined Carbohydrates and Dental Cavities

There's a definite association between the consumption of refined carbohydrates and dental cavities. Dr. Weston Price pointed this out in a number of transitioning societies in his epic work Nutrition and Physical Degeneration. Many other anthropologists and dentists have observed the same thing.

I believe, based on a large body of anthropological and medical data, that it's not just an association-- sugar and flour cause cavities. But why? Is it that they lack micronutrients-- the explanation favored by Price-- or do they harm teeth by feeding the bacteria that participate in cavity formation? Or both?

I recently found an interesting article when I was perusing an old copy of the Journal of Dental Research: "A Comparison of Crude and Refined Sugar and Cereals in Their Ability to Produce in vitro Decalcification of Teeth", published in 1937 by Dr. T. W. B. Osborn et al. (free full text). I love old papers. They're so free of preconceptions, and they ask big questions. The authors begin with the observation that the South African Bantu, similar to certain cultures Dr. Price visited, had a low prevalence of tooth decay when eating their native diet high in unrefined carbohydrate foods. However, their decay rate increased rapidly as modern foods such as white flour and refined sugar became available.

To test whether refined carbohydrates have a unique ability to cause tooth decay, the investigators took pieces of teeth that had been extracted for reasons other than decay (for example, crowding), and incubated them with a mixture of human saliva and several different carbohydrate foods:

• crude cane juice
• refined cane sugar
• whole wheat flour
• white wheat flour
• whole corn meal
• refined corn meal

After incubating teeth in the solutions for 2-8 weeks at 37 C (human body temperature), they had trained dentists evaluate them for signs of decalcification. Decalcification is a loss of minerals that is part of the process of tooth decay. Teeth, like bones, are mineralized primarily with calcium and phosphorus, and there is a dynamic equilibrium between minerals leaching out of the teeth and minerals entering them.

The researchers used teeth incubated in saline solution as the reference. The dentists were "blinded", meaning they didn't know which solution each tooth came from. This is a method of reducing bias. Here are some of the results. Cane juice vs. refined sugar:

Unrefined cane juice was not very effective at causing decalcification, compared to refined sugar. This was a surprise to me. Here is the result for wheat:Note that the scale is different on this graph. Wheat, and particularly refined wheat, is very good at decalcifying teeth in vitro. Corn:

Refined corn is much more effective at decalcifying teeth than whole meal corn. Next, the investigators performed an experiment where they compared the three types of refined carbohydrate to one another:
As one would predict from the graphs above, refined wheat is worse than refined corn, is worse than refined sugar. This is really at odds with conventional wisdom.

It's important to keep in mind that these results are not necessarily directly applicable to a living human being, who wouldn't let a mouthful of wheat porridge sit in his mouth for five weeks. But it does show that refining carbohydrates may increase their ability to cause cavities due to a direct effect on the teeth (rather than by affecting whole-body nutritional status, which they do as well).

The authors tested the acidity of the different solutions, and found no consistent differences between them (they were all at pH 4-5 within 24 hours), so acid production by bacteria didn't account for the results. They speculated that the mineral content of the unrefined carbohydrates may have prevented the bacterial acids from leaching minerals out of the teeth. Fortunately for us, they went on to test that speculation in a series of further investigations.

In another paper, Dr. T. W. B. Osborn and his group showed that they could greatly curb the decalcification process by adding organic calcium and phosphorus salts to the solution. This again points to a dynamic equilibrium, where minerals are constantly leaving and entering the tooth structure. The amounts of calcium and phosphorus required to inhibit calcification were similar to the amounts found in unrefined cane sugar, wheat and corn. This suggests the straightforward explanation that refined sugar and grains cause decay at least in part because most of the minerals are removed during the refining process.

However, we're still left with the puzzling fact that wheat and corn flour decalcify teeth in vitro more effectively than cane juice. I suspect that has to do with the phytic acid content of the grains, which binds the minerals and makes them partially unavailable to diffusion into the teeth. Cane juice contains minerals, but no phytic acid, so it may have a higher mineral availability. This explanation may not be able to account for the fact that refined sugar was also less effective at decalcifying teeth than refined wheat and corn flour. Perhaps the residual phytic acid in the refined grains actually drew minerals out of the teeth?

No, I'm not saying you can eat sugar with impunity if it's unrefined. There isn't a lot of research on the effects of refined vs. unrefined sugar, but I suspect too much sugar in any form isn't good. But this does suggest that refined carbohydrates may be particularly effective at promoting cavities, due to a direct demineralizing effect on teeth subsequent to bacterial acid production. It also supports Dr. Price's contention that a food's micronutrient content is the primary determinant of its effect on dental health.

Reversing Tooth Decay
Preventing Tooth Decay
Dental Anecdotes

Gluten-Free Dark Chocolate Chunk Cookies

Gluten-free chocolate chip cookies with chunks of dark chocolate.

My Ode to Cookies

Quick question. Which camp are you in? The You Can Never Have Too Many Cookie Recipes camp- or the Enough with All the Cookie Recipes contingent? You already know which faction I belong to. I don't even have to say it. In fact, I might even rename my culinary caucus. Something like, You Could Never In a Million Spectacular Carbon Infused Star Struck Years Have Too Many Cookie Recipes, Goddess Forbid.

Why all the cookie love? Life is short, number one. And just because I have celiac disease doesn't mean I surrender to a life without chocolate chip cookies and coffee laced cookies and mint chocolate chip cookies. I'm not giving up on warm-from-the-oven melty chocolate goodness. I'm most definitely not settling for any month old pre-packaged gluten-free poor excuse for a cookie. No way. Not gonna happen.

Because a good cookie is no small thing.

A good cookie can make you smile, even after a long, achingly crappy day. A good cookie might even bring you a kiss. Or little arms of appreciation wrapped around your neck. A good cookie might make you a new friend. Or prove to the class that you're not a total, allergic freak living on weirdo food that you have to feel sorry for and throw bread balls at.

A good cookie can make you feel like you belong.

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