Weight of the Evidence

Health = NY Obesity Tax

What smoking was for my parents’ generation, obesity is for my children’s generation.

Nearly one out of every four New Yorkers under the age of 18 is obese. In many high-poverty areas, the rate is closer to one out of three.

That is why, in the NY budget, there is a proposed tax on sugared beverages like soda. Research has demonstrated that soft-drink consumption is one of the main drivers of childhood obesity.

These days I’m no longer surprised when something like an “obesity tax” is foisted upon the masses without so much as a whimper – after all it is your fault if you’re fat, right? You should pay more, right?

Several commentators in the media applauded the move by the Governor of NY – Nicholas Kristof opined the hope that other states will follow suit because “if other states follow, it could help make us healthier.”

He even ties it up neatly with a bow, repeating the parallel to smoking and cigarettes, “These days, sugary drinks are to American health roughly what tobacco was a generation ago. A tax would shift some consumers, especially kids, to diet drinks or water.”

No one likes taxes, but by golly, we must do this for the children! We must save ourselves from ourselves with this tax – save the children, save the world, reduce consumption of sugared beverages and all will be well.

What’s maddening isn’t so much the proposed tax on sugared beverages, it is what government does if they can get away with it….what’s maddening is that no one seems to notice that we are already paying taxes that enable the flood of cheap soda, fruit drinks and sugared beverages into our markets.  It’s paid by our taxes in the Farm Bill, with corn being king amongst the crops subsidized by our tax dollars.

Obesity Tax

This new tax represents a double taxation to New Yorkers – taxed first from their income to subsidize corn in the Farm Bill; and now to add insult to injury, when they dare to consume products made from the corn products, their tax dollars helped make cheap at the consumer level – namely high-fructose corn syrup….beverages produced that are artificially low in price at the consumer level and often cheaper than buying a bottle of water!

If the government truly wants to tackle the obesity epidemic, perhaps it’s time to revisit the Farm Bill and how it is directly creating a market flooded with cheap corn calories at the consumer level for things like high-fructose corn syrup which is used in thousands of food products in our markets!

Weight of the Evidence

Low-Fat May Increase Relative Risk for Cardiovascular Events

Back in 2003, researchers decided to see how good the DASH Diet is compared to the Standard American Diet.

They designed a twelve-week trial with a two-week run-in where the diet over those two weeks contained 37% total fat with 16% of calories from saturated fat.

With 100 subjects participating, 50 were randomized to consume the DASH Diet while the other 50 were on their own to eat as they wished – this second group was the “control group.”

This particular study was well-designed – it not only sought to investigate the impact of diet on cholesterol levels, but also C-Reactive Protein (CRP), a marker of inflammation in the body that we understand is a pretty good predictor of cardiovascular risk – more so than cholesterol levels.

The DASH Diet really modified what the intervention group ate. Their diet contained just 27% total fat and just 6% saturated fat.

So, what happened after three months on this “better” diet?

Not much in the way of benefit. In fact, some findings were downright scary and the conclusions in the abstract only hint at how poorly some on the DASH Diet fared compared to the control group, “the presence of increased CRP was associated with less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet.

These findings document an additional mechanism by which inflammation might increase cardiovascular disease risk.”

Notice, the researchers don’t say anything in their conclusions about how we might need to re-think our dietary recommendations, especially in those with elevated CRP levels? How about I show you what happened, what the data actually tells us?

First, here is the full-text of the article Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial.

Those placed on the DASH Diet had median baseline cholesterol levels:

  • Total Cholesterol = 204.3
  • LDL Cholesterol = 131
  • HDL Cholesterol = 48.7
  • Triglycerides = 89.48
  • TC/HDL Ratio = 4.2
  • LDL/HDL Ratio = 2.6

When the group was divided into those who had a baseline CRP below or above the median the results were indicative of how damaging a low-fat diet can be. For those with CRP below the median CRP of 2.37 the following happened:

  • Total Cholesterol = 176.47
  • LDL Cholesterol = 110.29
  • HDL Cholesterol = 45.66
  • Triglycerides = 90.37
  • TC/HDL Ratio = 3.86
  • LDL/HDL Ratio = 2.4

No one can argue – they did pretty good. Not blow your socks off impressive, but they didn’t get appear to get worse and their TC/HDL and LDL/HDL Ratios did improve slightly.

Keep in mind though, the diet did nothing to reduce their level of CRP though. We’ll get to that in a moment. For now, let’s see how those with CRP levels above the median fared…

  • Total Cholesterol = 201.63
  • LDL Cholesterol = 130.03
  • HDL Cholesterol = 46.44
  • Triglycerides = 110.75
  • TC/HDL Ratio = 4.34
  • LDL/HDL Ratio = 2.8

This “unfavorable outcome” on these subjects’ health occurred in just three months and the best the researchers could do is bury it in the full-text rather than make it very clear in their abstract that the difference isn’t just the minor inconvenience of “less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet” but statistically significant differences that had real potential to negatively impact health if such changes continued with eating such a diet over the long-term.

Not only did the diet result in an “unfavorable outcome” for these individuals, but when it did not change their CRP level that means that this change increased their relative risk for a cardiovascular event – basically increased their risk to have a heart attack.

Let’s explore why the CRP levels were important here – not just for those with above the median levels, but also those below the median. First, the researchers interpretation that those with CRP below the group median had a favorable outcome with the diet is misleading in my opinion. While the diet did have an effect on cholesterol levels and ratios, it had NO EFFECT on the CRP levels of the subjects following the DASH Diet.
The abstract states this “The DASH diet, net of control, had no effect on CRP.”

If we use Ridker et al’s assessment of risk, developed in the New England Journal of Medicine publication of Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events, we find that the baseline risk of those assigned the DASH Diet was a relative risk of 2.9. That is, when they started the DASH Diet they already had a 2.9 times greater risk of a cardiovascular event than someone with a “normal” CRP value of 1.6 or less. Let me be clear here – 1.6 may even be considered high if we use the Framingham data as a benchmark, but for now, let’s stick with the Ridker et al method to assess risk.

Because their CRP didn’t change, even the change in their cholesterol and TC/HDL didn’t improve their relative risk. It actually made it worse! We must consider that the diet did not change their CRP level when determining risk here and use the value they used – 2.37. In Ridker et al’s assessment protocol, that level combined with a TC/HDL ratio of 3.86 translates to a relative risk of 3.5 times greater risk of a cardiovascular event than someone with a “normal” CRP value of 1.6 or less. Did you catch that? The relative risk increased from 2.9 to 3.5!

For those who had a CRP above the median, we again must maintain no change in CRP from baseline, as the data suggests. Here, the change in risk is dramatic because the TC/HDL Ratio changed so much. For those eating the DASH Diet who had a CRP above the median, the resultant change in their TC/HDL Ratio increased their relative risk to a 4.2 times greater risk of a cardiovascular event than someone with a “normal” CRP of 1.6 or less. Their relative risk increased from 2.9 to 4.2!


Let me be clear here – Ridker et al published their work almost a year before this DASH Diet trial – yet the researchers didn’t even consider discussing the implications of the findings in terms of relative risk. Instead, they couched their words with phrases like “less favorable” and “likely relationship” between diet and lipids without any real fear the DASH Diet might not just cause an “unfavorable” outcome in terms of lipid values (cholesterol readings) but real-world problems, like an increased relative risk for cardiovascular events!

Ridker et al aren’t the only ones to find such a disturbing relationship with CRP and relative risk either!

In October 2001, the International Journal of Obesity and Related Metabolic Disorders published findings from Pannacciulli et al, C-reactive protein is independently associated with total body fat, central fat, and insulin resistance in adult women. Their findings – Our study has shown an independent relationship of central fat accumulation and insulin resistance with CRP plasma levels, thus suggesting that mild, chronic inflammation may be a further component of the metabolic syndrome and a mediator of the atherogenic profile of this syndrome.

In June 2001, the journal Atherosclerosis, published The association of c-reactive protein, serum amyloid a and fibrinogen with prevalent coronary heart disease–baseline findings of the PAIS project, which concluded that “CRP, SAA and fibrinogen, which are markers of inflammation, were positively and significantly associated with prevalent CHD.”

So the concept that CRP is a valuable marker and when measured should be used as part of an assessment of risk isn’t really a stretch here. The researchers failed to acknowledge its potential importance, the increased relative risk even in those with CRP below their baseline measure and especially in those with CRP above their baseline measure.

Their simple conclusion that some realize a less benefit from the DASH diet totally fails to recognize that neither group reduced their relative risk for a cardiovascular event – in fact, both groups had an increased risk after three months – one group more so than the other – but both still increased their risk!

And now, some three years later, with even more trials completed, even more data showing the same miserable effects, we’re still being told that DASH and other low fat dietary approaches are better for us!

Better than what? Perhaps better at increasing relative risk?

he data shows they’re no better or worse than the Standard American Diet – which I’m sure you’ll agree is certainly not leading us to better health and quality of life long-term. So then, what exactly is a low-fat diet better than since almost every trial is comparing it to the Standard American Diet? I know I’d like to know.

We’re told it’s better, but for some reason no one can tell what it’s better than – and don’t forget we’re not told about the risks to many of us from these “better” diets – risks that are clear as day when you look at the data and not just rely on the basic information in the abstract! Not a peep from the AHA about this finding or any caution about how this dietary approach – DASH – may really negatively affect someone with a high CRP level.

Don’t you think it’s time we took this stuff seriously and actually looked for a dietary approach that works as promised – ya know, one that does optimize health and well-being over the long-term, that does reduce the risk of disease and premature death and that is based on evidence instead of prevailing dogma?

Weight of the Evidence

Fat, Cholesterol, LDL, HDL Discussion

For decades a diet that is higher in fat than recommended – that is more than 30% of calories from fat and more than 10% from saturated fat – has been implicated as a “cause” of high cholesterol, which in turn has been implicated as a “cause” of cardiovascular disease.

Remember in school the equation problem “A=B, B=C, so A=C?”
When it comes to cholesterol, the equation is fairly simple and straight-forward:

  • More than 30% of calories from fat = risk of high cholesterol
  • High cholesterol = risk of cardiovascular disease
  • More than 30% of calories from fat = risk of cardiovascular disease

But, it is true?

For years research data has continued to find contradictory results when extrapolating data on diet and cholesterol and heart disease. When data supports the idea, the media is all over it…when the findings are weak or in contradiction to the idea, the findings are often ignored, discredited, or some flaw is found in the design to explain the contradiction. Then, there is the “paradox” explanation – namely the “French Paradox” and the “Spanish Paradox” – advanced when nothing else can explain away findings.

New findings, reported today by Reuters Health in the article, “Genes key in how diet affects cholesterol levels” challenge the conventional wisdom of “diet = high cholesterol.”

The study of 28 pairs of male twins — one a lean athletic type, the other a bit rounder and sedentary — found that brothers tended to show the same cholesterol response to high-fat and low-fat diets, even though their exercise habits were starkly different.

Because identical twins share the same genetic makeup, the findings point to the importance of genes in determining how a person’s cholesterol levels respond to diet and lifestyle changes, according to the study authors.
The study followed 28-pairs of identical twins (male) and used cross-over diets containing different amounts of fat. One diet had 40% of calories from fat, the second had 20% of calories from fat.


The study found a high degree of similarity in how brothers’ LDL Cholesterol (the “bad” form of cholesterol) responded to the switch from the high-fat diet to the low-fat one. On average, the men’s LDL declined on the low-fat diet, but any individual’s response seemed to depend largely on genes.

In general, low-fat diets tend to lower LDL concentrations, but can also decrease “good” HDL cholesterol and raise triglycerides, another type of blood fat. So cutting dietary fat may not have a net benefit, depending on the individual.

What the article didn’t state was that some of the twins followed did better with a higher fat diet than a lower fat diet. Add to that the finding that HDL may decrease while triglycerides increase on a low-fat diet – those observations are noteworthy and future research must explore why. HDL is basically the “garbage collector” of cholesterol. The evidence to date supports the contention that high triglycerides are a risk factor. When a dietary change impacts both negatively, this should be a red flag!

For those who fail to better their cholesterol profile with diet, genes — rather than a lack of will — could be the reason, said Paul T. Williams, a researcher at the Lawrence Berkeley National Laboratory in California and the study’s lead author.

Controlled-carb diets have been shown to markedly improve cholesterol levels in people following them in controlled-studies. This is not to say everyone benefited – there is a population whose cholesterol responds negatively to a higher-fat, low-carb diet.

Some studies suggest this population could be as high as 30% of the general population.
For this reason, it is critical that you have your cholesterol profile followed by a physician if you modify your diet to be low-carb or, with these findings that show HDL and triglycerides may be negatively impacted by a low-fat diet if you go that route.

Until, or unless cholesterol levels are ruled out of the equation as a risk factor, it is important to have your cholesterol checked with any dietary change. If you’re not seeing a positive result in your cholesterol profile work with your doctor to adjust your macronutrient intake to see if a different one works better.