Strange Science: Meat consumption increases risk of Type 2 diabetes

A new meta-analysis concludes that a diet high in meat increases your risk of Type 2 diabetes by 17%.  Eating a lot of so-called "red" meat was associated with a slightly higher increase (21%), and a high intake of processed meats increases your risk by a whopping 41%.

Media reports are quick to point out that this is just the latest in "an ever increasing list of bad news for red and processed meat."

In all of these studies, the division of meat into "red" and "white" seems totally arbitrary, as I discussed at length in this post: Meat and mortality: What does color have to do with it? 

In this particular case, the authors concede that the apparent association between meat consumption and diabetes risk could be explained by other factors. (So why exactly are we going to press with this result?)

A false association seems even more likely in this case than in the recent associations between meat intake and cancer risk or all-cause mortality.  At least there are plausible mechanisms to explain why high meat intake might increase cancer risk. For example, charred meat contains known carcinogens--although I hasten to point out that this has nothing to do with the "color" of the meat.

Diabetes is a disease of disordered carbohydrate metabolism. Meat is made up of protein and fat. How could eating more protein and fat increase the risk of diabetes?  Doesn't it seem more likely that there is something else about the lifestyle or dietary habits of people who eat large quantities of meat (especially processed meat) that might increase their diabetes risk? Are they also over-weight? Are they sedentary? What's their consumption of alcohol? Of high-glycemic foods? 

I'm keeping an open mind but pending more convincing data, I'm not sure I'm buying it.

Reality Check: Does candy turn kids into monsters?

Trying to rein in the amount of sugar kids eat is hard enough.  Having a plastic pumpkin full of candy in the house sure doesn't make it any easier.

There are plenty of compelling reasons to limit kids' intake of sugar. Candy is a source of empty calories that can displace more nutritious foods, lead to weight gain, and wreak havoc with insulin metabolism. (Type 2 diabetes used to be called Adult Onset Diabetes, but no more.)

But many parents are also convinced that sugar turns kids into little monsters--making them hyper-active, aggressive, or otherwise unmanageable. Yet the research fails to bear this out.

Is it all in parents' heads? 

Controlled studies have measured the effects of sugar consumption on behavior and cognitive performance and failed to find any connection. See for example this meta-analysis. There have even been interesting studies where parents were asked to observe kids behavior. When the parents thought the kids had eaten sugar, they reported changes in behavior--even when the kids had actually been given a placebo. See this article for more on the sugar-hyperactivity myth.

Just last month, there was an interesting new twist on this: Researchers found that kids who ate candy every day were more likely to be arrested as adults for crimes involving violence, as reported by AP News. The researchers hastened to add that the association is probably more complex than it sounds. It may be, for example, that individuals with poor impulse control eat more candy as kids and then commit more crimes as adults. 

What's a responsible parent to do?

Most parents settle for damage containment and try to strike a balance between nutrition concerns and letting kids enjoy this once-a-year festival. Rather than banning all Halloween candy (now who's the monster?), try to limit the amount that is collected and then dole it out slowly.  One small treat after a healthy meal isn't going to turn your kids into monsters.  Getting your kids up and moving--whether it's to rake leaves, play touch football, or even some Wii tennis--is also an effective way to mitigate the effects of a little extra sugar.  

Common sense prevails: Froot Loops not a "Smart Choice"

An industry-funded labeling program which awarded green "Smart Choice" checkmarks to packaged foods, based on "strict science-based nutrition criteria" has been suspended after the FDA questions its validity. 

And rightfully so.  Any system that considers Froot Loops cereal to be a smart choice is worse than meaningless. Read more here.

Can you absorb fat-soluble vitamin D from skim milk?

Q. I recently read that Vitamins A, D, E, and K are fat soluble, meaning that they dissolve in fat instead of water. Does this mean that these vitamins need to be eaten with some type of fat source for the body to absorb them? For instance, if somebody ingested just a cup of skim milk would any of the Vitamin D not be absorbed because of the lack of fat?

A. It's not so much that fat-soluble vitamins dissolve in fat, but that they are carried across the intestinal cell barrier by lipid (fat) molecules.  So, while it is true that fats are necessary for transport and absorption of fat-soluble vitamins, it doesn't take much!

A couple of years ago, there was a study that found that eating avocado with vegetables increased the absorption of fat-soluble beta-carotene from the vegetables. However, a study that looked specifically at vitamin D found that vitamin D was absorbed just as well from both skim milk and orange juice as it was from whole milk. (Maybe the fiber in the vegetables plays a role somehow?)

The most likely causes of fat-soluble vitamin deficiency includea missing or malfunctioning gall bladder, bariatric (weight loss surgery), intestinal resection, or other serious digestive diseases that interfere with absorption of fats.

Homocysteine and heart disease

You don't hear a whole lot about homocysteine these days but ten or fifteen years ago it was quite the buzzword in nutrition and preventive medicine circles--and a cash cow for nutritional supplement sellers.

A little background on the homocysteine hypothesis

Population studies (aka epidemiological studies) showed that people with high levels of homocysteine in their blood had a higher risk of heart disease. Homocysteine is an amino acid which is an normal byproduct of protein metabolism. Ideally, it is further converted into another amino acid, methionine. However, if this "recycling"  breaks down, homocysteine can build up in the blood. 

When the link between high homocysteine and heart disease risk was noticed, researchers theorized that homocysteine might irritate the blood vessel lining, leading to injury, inflammation, and the formation of arterial plaques.

Certain B vitamins (B6, B12, and folic acid) act as co-factors in the conversion of homocysteine to methionine. Further research confirmed that those with high homocysteine tended to be low in one or more of these nutrients. Taking the next step, it was established that supplementing with these nutrients reliably reduced elevated homocysteine levels. It seemed all but certain that this would in turn lower heart disease risk.

Hold that thought

However, the homocysteine hypothesis recently took a big hit, in the form of a meta-analysis of eight studies involving some 24,000 subjects. The upshot? The authors found “no evidence that homocysteine-lowering interventions, in the form of supplements of vitamins B6, B9 or B12, given alone or in combination, at any dosage compared with placebo or standard care, prevents myocardial infarction, stroke, or reduces total mortality in participants at risk or with established cardiovascular disease.”

Ouch.

Those in the business of selling nutritional supplements are crying foul, claiming that the conclusions are "misleading."  Read responses from the Health Food Manufacturers’ Association (HFMA) and the International Alliance of Dietary/Food Supplement Associations (IADSA).

It's possible that those with very high homocysteine levels have more to gain than those with only mildly elevated levels--and that the meta-analysis obscures this reality. The meta-analysis also failed to evaluate whether B vitamins could prevent healthy people from developing heart disease. But, coming from organizations who profit from sale of dietary supplements, I find this argument less compelling.

I'm curious: How many of you have had your homocysteine levels tested? How many of you take B vitamins specifically to manage homocysteine levels? Share your comments below.

High cholesterol no cause for worry?

Q. I am a 24-year-old female. I'm a normal weight (5'7", 133 lbs). I work out at least 5 days per week. I  avoid all processed food and generally try to fill my days with whole grains, veggies, fruits and non-fat dairy sources. I usually have a small amount of caffeine in the mornings, I don't smoke, and I drink two or three times per month. All in all, I think I lead a pretty healthy lifestyle. However, I went to my doctor last week and was surprised to find that my cholesterol is slightly high (more than 200 mg/dL). I don't have a family history of high cholesterol or heart disease.  Is this a common problem in people who lead otherwise healthy lifestyles? I'm hoping to avoid taking prescription meds for the rest of my life.

A. I think it's a little soon to be thinking about prescription meds for life!!  Given all you've reported here, you may not have anything to worry about.  For one thing, high cholesterol does not mean you have (or will develop) heart disease.  Although elevated cholesterol is statistically linked to a higher incidence of heart disease, many people who die of heart disease have normal cholesterol...and many people with elevated cholesterol never get heart disease.  Cholesterol tests are screening tools, not diagnostic ones.

Cholesterol is only one piece in a larger picture. Given the rest of the details you've given (normal weight, not sedentary, no family history of heart disease or high cholesterol, normal blood pressure), your statistical risk of developing heart disease in the next ten years is extremely small. 

I'm also wondering about the details of your cholesterol--specifically about the break-down of HDL ("good") and LDL ("bad") cholesterol.  Your total cholesterol may be high because your HDL is high, thanks to all your healthy habits.   I would think before prescribing medication, your doctor would follow up with a more comprehensive lipid panel. I'd give even odds that a retest would show normal cholesterol, anyway. The slightly high reading may well have been an anomaly.

Finally, it sounds as if your diet is very low in fat and fairly high in carbohydrates.  If you wanted to see if dietary modifications might nudge your cholesterol numbers in the right direction (although, again, I'm not sure you really have that much to worry about), you might try adjusting the balance of your diet to be a little higher in fat and lower in carbs, particularly grains. Olives, olive oil, almonds, and avocados (all rich in monounsaturated fats) would be good choices.

Let us know what happens next.

 

Too much saturated fat during pregnancy sets kids up for obesity? Let's not jump to conclusions

Here's what the study found: If you feed a pregnant mouse a high-fat diet, the mouse's offspring are more susceptible to fatty liver disease. (Access the journal article here.)

Here's how it was reported to the media: Women eating a diet high in saturated fat during pregnancy increase the risk of fatty liver disease in their children. (Read the press release here.)

Cue senseless panic among pregnant women everywhere and a new old wives' tale about the dangers of eating saturated fat during pregnancy.

The press version never mentions that the study was done on mice. In fact, the use of the words "woman," "mother," and "child" to describe the mice creates the strong false impression that this research was done on humans.

Furthermore,  the study compared high-fat versus normal-fat rat chow, not saturated versus other types of fat. The word "saturated" doesn't appear anywhere in the published study. So why should we conclude that saturated fat is any worse than any other type of fat?

It's a shame when worthwhile research gets undercut by sloppy, irresponsible reporting. But it's not just the media. Researchers giving sensational, misleading quotes to the press are a big part of the problem--and they should really know better.

Purslane as a source of omega-3: a reality check

Q. Why does Nutrition Data show purslane as having no omega-3 fatty acids, when it is very high in omega 3?

A.  First a quick clarification: When a value is known to be zero, you'll see a "0".  The tilde symbol "~" indicates an unknown value. So, our listing doesn't indicate that purslane has no omega-3 fatty acids, it indicates that the amount of omega-3 fats are unknown.  (For more on this unfamiliar vegetable, see this post: "On today's menu: Weeds.")

But this still raises an interesting question:

Why wasn't omega-3 content in purslane measured?

The USDA's nutrient data lab doesn't test every food for every nutrient. It would be a waste of time and money, for example, to analyze carrots for cholesterol because plants don't contain cholesterol. But when a food is known or thought to be high in a particular nutrient, that nutrient usually is included in the analysis.

Purslane has gained a reputation as being a good source of omega-3 fatty acids. An oft-cited 1992 analysis, published in the Journal of the American College of Nutrition, found that 100 grams of purslane contained 300-400 mg of omega-3 fats.

But if you search the scientific literature, you'll see that the amount of omega-3 fats in purslane varies a LOT, depending on the variety, the age of the plant, the part of the plant you analyze (leaves, stems, seeds), and the time of harvest. The purslane analyzed in the 1992 study was clearly at the high end of the range. The purslane analyzed at the Nutrient Data Lab appears to be the low end--but is comparable to other published analyses.

The purslane analyzed by the NDL contained only 1mg of fat per gram, or about one tenth of one percent.  With such a low percentage of total fat, it didn't really make sense to break that down further into individual fatty acids.

Is purslane a valuable source of omega-3 or not?

It's true that, compared to other green vegetables, purslane is rich in omega-3 fatty acids. About half the fat in purslane is omega-3. But green vegetables are very low in fat, so that doesn't add up to much.

Let me put this in perspective for you: Even if you were lucky enough to got some high octane purslane like the stuff analyzed by Simopoulos in 1992, you'd need to eat 4 pounds of it to get the amount of ALA found in one tablespoon of flaxseed oil.  Hope you're hungry!

How much omega-3 is too much?

Q. Is there any upper limit as far as how many grams of omega 3 you can take? I'm aiming for an omega-6 to omega-3 ratio of 4:1.  As an example, if I ate 10g of omega 3 and 40g of omega 6, that's still in the 4:1 ratio but is 10g of omega-3 too much? What would be the upper limit?

A. There is no UL (tolerable upper limit) for omega-3 or omega-6 fatty acids (PUFAs).  The USDA feels it has "insufficient evidence" to set one. Instead, you might want to consider how much total fat you're going to eat and how you want to divide that up. For example, consuming large amounts of PUFAs might either cause you to miss out on the benefits of other fats, such as monounsaturated fats, or lead you to eat too much total fat.

Many experts recommend that PUFAs should make up 5-10% of your dietary calories and that seems reasonable to me.  The rest of your fat calories would come from monounsaturated fats like those found in olives and avocados and/or saturated fats from meat, dairy, and tropical oils.  Trans fats from hydrogenated oils and fried foods should ideally be kept to an absolute minimum.

In your example, you'd be eating 50g of PUFAs, for a total of 450 calories. Unless you're eating 4500 calories a day, that might be a little out of balance.  Without knowing the particulars of your situation, sounds as if you might want to think about ratcheting your intake of BOTH kinds of PUFAs back a bit.

Building your dietary fat "profile"

Here's how a healthy distribution of fats might look for a typical person eating 2500 calories a day:

30% of calories as fat = 83 g 

Of that:

    15% of calories from monounsaturated fat = 40g

    7% of calories from saturated fat = 20g

    7% of calories from polyunsaturated fats = 20g

To maintain a 4:1 ratio of omega-6 to omega-3, that would be 16g omega of omega 6 and 4g of omega 3.

Fish or flax?

As far as the dangers of taking too much omega-3, it depends whether you're talking about 10g of flax oil, which provides alpha-linolenic acid (ALA), or 10g of fish oil, which contains the much more biologically active forms of omega 3 (EPA and DHA). 

Ten grams of fish oil could potentially create some issues, such as interfering with blood-coagulation and immune function (not to mention digestive distress). Whether or not these might be concerns for you is a question for a licensed nutrition professional who knows the details of your situation.

       

   

Do overweight people eat less than thin people (or do they just think they do)?

A lot of people are excited about Gary Taubes' book Good Calories, Bad Calories, which claims that weight loss or gain has nothing to do with how many calories you eat but how much refined carbohydrate you eat. I heard Taubes present his ideas at a conference last year and he makes some great points. Ultimately, I agree with his conclusion--over-consumption of refined carbohydrates is a primary cause in today's epidemic of "diabesity."

But I think he over-argues his case--and some of his arguments about how and why carbohydrates lead to obesity are flawed.

For example, as proof that excess calories are not the cause of weight gain, Taubes cites studies showing that that overweight people eat the same or less than thin people. Here's the problem: The studies he cites use self-reported intake records. We know that overweight people consistently under-report the number of calories they eat. (Here's yet another study measuring this.) The more overweight you are, the more you tend to under-report.

In fact, when you put overweight people into controlled (i.e. in-patient) settings and feed them the number of calories they think or say they are eating, they reliably lose weight--regardless of whether they are eating refined carbohydrates or not. (Whether this weight loss is sustainable in the real world is another question).

I think it's more accurate to say that refined carbohydrates seduce us into eating more calories than we need.  They taste good, you can consume a lot of calories before you get full, and you're hungry again sooner than you would have been had you eaten proteins, fats, or non-refined carbs. Excess calories = weight gain.

Eliminating or reducing refined carbohydrates may help realign your appetite regulation systems with your actual energy needs.  Reduced calories = weight loss.