Some predictions suggest that “people suffering from severe obesity (BMI > 40) is predicted to more than double, from 5 to 11 percent.” Think the health care costs are unsustainable now? They are only going to get worse if we don’t turn things around ASAP.
http://www.dietdoctor.com/fat-forecast-disaster
Alzheimer's Brain: (via thehealthage.com)
As if you needed another reason to lay off the highly-processed and sugary foods and to keep insulin levels in check, a new study has shown that insulin resistance can lead to cognitive decline because of the brain’s inability to maintain proper glucose uptake: (via Science Daily).
I recently posted an article on Facebook regarding an experienced heart surgeon’s opinion on the problems with the current paradigm driving the medical community that high fat–with saturated fat being specifically demonized–causes cardiovascular disease (CVD). I agreed with the surgeon’s opinion, and therefore felt comfortable posting the article to raise some awareness of the growing opinion he expresses: “The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated…Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes.” However, I realized that these types of posts are rarely productive because they are so easy to ignore, and also because such articles make assertions that seem equally as spurious as the paradigm they are fighting against.
So, despite all the “knowledge” of conventional wisdom mounted against me, and the near impossibility that anything productive will come of this post, I would like to get most of my current ideas posted–most of which are the result of reading far better researchers than myself–about the Lipid Hypothesis of Cardiovascular Disease (CVD). Luckily, guys like Martin Berkhan at Leangains, Chris Masterjohn, Mark Sisson at Mark’s Daily Apple, and an increasing number of physicians and researchers (’bout time!) have got my back.
CAVEAT: I will try to make this article as self-explanatory as possible, but be aware that there are many links contained herein to many different authors who have done a much better job than I will at assessing the research. The purpose of this article is my attempt is to pull together their analyses and conclusions, and to offer any little advice of my own that I may have.
To begin, one thing I would like to go ahead and get out of the way is the assumption that saturated fat causes CVD. Not is correlated, not may play some role in the development of CVD, I mean the erroneous claim that if you eat a lot of saturated fat, you will be at a significant risk of developing heart disease. Also note the American Heart Association (AHA) recommendation to “replace foods high in saturated fats with foods high in monounsaturated and/or polyunsaturated fats,” as I will address the problem with this recommendation in this discussion. This meta-analysis titled “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease” should help me begin to dispense with this myth (Siri-Tarino, et al., 2010). Their conclusion:
Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.
In fact, the accepted mechanism that “saturated fat = CVD” is so mistaken, that there is plenty of evidence to suggest that the opposite is the case. For example, a recent study has found the exact opposite association: higher saturated fat consumption was correlated with lower CVD incidence. Some quotes to keep you from having to link to all these studies:
In our studies of simple hypercholesterolemia in men, a fat intake <25% of energy and a carbohydrate intake >60% of energy was associated with a sustained increase in triacylglycerol of 40%, a decrease in HDL cholesterol of 3.5%, and no further decrease in LDL in comparison with higher fat intakes (5). In contrast, a low-fat diet in persons with combined hyperlipidemia caused no worsening of triacylglycerol or HDL, but intakes of fat >40% of energy and of carbohydrate <45% of energy for 2 y were associated with a lower triacylglycerol concentration at a stable weight (6)… Modest favorable trends in triacylglycerol and HDL-cholesterol concentrations were observed with higher fat intakes.
When translated to English, that first sentence means that a low fat and high carbohydrate diet increases triacylglycerol, which has been linked to increased risk for CVD. Also, this diet caused decreased HDL (“good”) cholesterol and no change in LDL (supposedly “bad”) cholesterol compared to high fat intakes. Well, that’s a bit of a head-scratcher. I thought the AHA recommended just this diet to decrease risk for heart disease. I repeat, the low fat, high carbohydrate diet seems to increase the risk factors for CVD (elevated triacylglycerol), decrease protective factors (“good” HDL), and cause no change in known associated risk factors such as LDL cholesterol. Uh oh… Here’s how Mozaffarian et al sum everything up (italics are my emphasis):
In conclusion, the hypothesis-generating report of Mozaffarian et al draws attention to the different effects of diet on lipoprotein physiology and cardiovascular disease risk. These effects include the paradox that a high-fat, high–saturated fat diet is associated with diminished coronary artery disease progression in women with the metabolic syndrome, a condition that is epidemic in the United States.
Well that sure is confusing…but before we throw the baby out with the bath water, surely we can maintain that lipid consumption plays some role in CVD, but perhaps the problem is our incomplete picture of it? As it stands, the hypothesis saturated fat causes heart disease seems to be on pretty feeble ground.
***VERY BRIEF DIGRESSION***
Just for fun–and because I’m a bit of a foodie and lover of French food–I also want to briefly mention The French Paradox (high sat. fat consumption and low CVD death rates in France) to further erode the foundation upon which the saturated fat to CVD linkage currently stands. I concede that this paradox has numerous potential confounds as described here (Ferrieres, 2004):
In correlation studies, measures that represent characteristics of an entire population (consumption of animal fat, daily milk, and alcohol) are used to describe disease (CHD mortality). Limitations of correlational studies are the inability to link exposure with disease in particular individuals, the lack of ability to control the effects of potential confounding factors.
However, it’s amazing how wary researchers can be of any confounding factors involved a study that threatens to challenge the paradigm, yet they seem to remain completely unaware of confounding factors that helped to establish said paradigm. For example, Martin Berkhan at Leangains and many other researchers have pointed out that the study that kicked off all this ridiculous confirmation bias–back in the 1960′s, Ancel Keys’ study selected data to support his conclusions while throwing out all the data that did not support his conclusions, thus becoming the first study to link CVD with cholesterol consumption…For an amazingly comprehensive refutation of the Lipid Hypothesis and the problems of the Ancel Keys study, consider reading Gary Taubes’s tome Good Calories, Bad Calories.
***OK, BACK ON TRACK***
With that association out of the way–and hopefully with your recognition of the complexity involved–let’s move on.
In defense of Dr. Dwight Lundell’s claim “Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes…”, I suggest reading Chris Masterjohn’s article titled “High Cholesterol And Heart Disease — Myth or Truth?” The beauty of this article is that it is so lucidly written that it manages to: (1) lay out the series of experiments that helped establish the current Lipid Hypothesis; (2) make sense of the long-established correlations between blood cholesterol in heart disease; (3) address problems with the Lipid Hypothesis based on what we know about cholesterol metabolism, and how the susceptibility to oxidation of different lipids–specifically sat. fat vs. polyunsaturated fats (PUFAs)–is often a neglected aspect of nutrition recommendations. I repeat, if there is one link in this entire post that is worth reading, it is this one; he outlines the historical progression of the Lipid Hypothesis, and intelligently discusses the relevant biochemistry in a clear manner. Mr. Masterjohn’s comment in his conclusion section is particularly telling of the problems with the narrow-minded Lipid Hypothesis: “So is the lipid hypothesis correct? Not in its original form. The weight of the evidence clearly supports a role for the oxidation of LDL and not the concentration of LDL in the blood in the development of atherosclerosis.” The sections titled “The Role of Oxidized LDL in Heart Disease” and the subheading “Oxidized LDL and the PUFA Connection” are also very interesting, as they relate to the extremely problematic USDA recommendations that call for replacing saturated fats with polyunsaturated fats (e.g. vegetable oils and soybean oil).
His final summation shows how our current picture of how most people understand CVD is too simplistic:
So, does cholesterol cause atherosclerosis? No!
But do blood lipids? Yes. Atherosclerosis is a disease in which degenerating lipids infiltrate the blood vessel wall and cause inflammation and degeneration of the local tissue once they arrive there. Solid evidence has amassed in favor of this view for the last 100 years.
Recent studies Dr. Lundell’s claim of the importance of inflammation as a factor associated with CVD. Such a study, done by Rodondi et al. (2010), claims that markers of inflammation such as IL-6–a cytokine released by the immune system to facilitate pro- and anti-inflammatory responses–could be important predictors of CVD risk:
Our findings are consistent with previous studies on the association between inflammatory markers and CHD in older adults (15, 28) and on single markers of atherosclerosis (3, 17, 29), but our results add information on the direct comparisons of both markers of inflammation and markers of atherosclerosis… In summary, our study suggests that IL-6 and AAI are associated with future CHD events and help improve cardiovascular risk prediction beyond traditional risk factors in the elderly, with modestly improved risk reclassification…This study suggests that new risk scores that include IL-6 or AAI might improve CHD prediction and risk stratification in the elderly.
With this is mind, it might be a smart decision to increase antioxidant consumption to reduce PUFA oxidation, thereby reducing the potential for systemic inflammation in the body. An additional intervention may be to go back to the way grandma used to cook, and put butter back in place of margarine. Besides, all that enthusiasm of replacing butter (high saturated fat) with margarine (high PFA content) was short-lived, given the horrible health consequences. Oops…
To conclude, let’s take stock of what we have considered:
The arguments above provide evidence to contradict the current Lipid Hypothesis of CVD, which has become about as widely accepted in American nutritional guidelines as the knowledge the Earth is round (save a few scattered Flat Earth cults). With our current knowledge of the significantly greater susceptibility of PUFAs for oxidation, it seems decreasing sat. fats and increasing PUFAs may in fact be the exact opposite recommendation one should make for decreasing CVD…I’m not going to tell anyone else what to eat, but I’m going to have to pass on the fat-free bagels and instead continue to eat my bacon and eggs for breakfast, especially if I can obtain them from the most natural, free range sources possible.
References
Berkhan, Martin (2010) Diet Mythology: Ancel Keys and the Fat Fallacy. Leangains.com. http://www.leangains.com/2010/06/diet-mythology-ancel-keys-fat-fallacy.html.
Ferrie`res, Jean (2004) THE FRENCH PARADOX: LESSONS FOR OTHER COUNTRIES. Heart; 90:107–111.
Knopp, Robert H and Barbara M Retzlaff (2004) Saturated fat prevents coronary artery disease? An American paradox1,2. Am J Clin Nutr; 80:1102–3.
Libby, Peter (2006) Inflammation and cardiovascular disease mechanisms1–3. Am J Clin Nutr; 83(suppl):456S– 60S.
Masterjohn, Chris (2008) High Cholesterol And Heart Disease — Myth or Truth? cholesterol-and-health.com: Uncovering the truth about America’s most demonized nutrient. http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html.
Rodondi, Nicolas, Pedro Marques-Vidal, Javed Butler, Kim Sutton-Tyrrell, Jacques Cornuz, Suzanne Satterfield, Tamara Harris, Douglas C. Bauer, Luigi Ferrucci, Eric Vittinghoff, and Anne B. Newman for the Health, Aging, and Body Composition Study (2010) Markers of Atherosclerosis and Inflammation for Prediction of Coronary Heart Disease in Older Adults. American Journal of Epidemiology; Vol. 171, No. 5: 540–549.
“Saturated Fats Q&A”. Getting Healthy. American Heart Association. http://www.heart.org/HEARTORG/GettingHealthy/FatsAndOils/Fats101/Saturated-Fats_UCM_301110_Article.jsp#.T23rrczk9yg.
Siri-Tarino, Patty W, Qi Sun, Frank B Hu, and Ronald M Krauss (2010) Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease1–5. Am J Clin Nutr; 91:535–46.
Sisson, Mark (2012) How Might Inflammation Cause Heart Disease? Mark’s Daily Apple. http://www.marksdailyapple.com/how-might-inflammation-cause-heart-disease/#axzz1q34Xrnar.
Interesting video by Richard Dawkins talking about what one’s ancestors would look like 185 million generations ago. If this seems too insane to be true, take a second to really consider the thought experiment: 185 MILLION generations. I’m no so sure about my math in terms of the rate of reproduction, but I’m guessing this would probably bring us close to 1 BILLION years. Some religious fundamentalists suggest the Earth is approximately six thousand years old. Needless to say, this does not give us a realistic picture of human origins based on our well-supported scientific consensus. I want to repeat a section from my previous post Chipping Away at the Human Ego because I these misunderstandings and misinformation is one of the primary reasons that people don’t accept evolution: they don’t understand it, and they have been given erroneous information that claims to dispute it. From my post, Chipping Away at the Human Ego: “To put this even further in perspective, consider the quote from the article in The Guardian written by Richard Dawkins discussing the comically immense magnitude of error of a creationist (named McIntosh in the article), who suggests the Earth is less that 10,000 years old:
We of the “establishment” think the Earth is 460,000 times older than McIntosh’s estimate. It is as though McIntosh estimated the height of a man as 6 feet and then accused the rest of us of believing that the same man was 460,000 times as tall, or 521 miles. Or, looking the other way, it is as though McIntosh looked at the establishment geographers’ measurement of the distance from New York to San Francisco and claimed that the true distance from sea to shining sea was 460,000 times smaller, namely about ten yards. Maybe McIntosh is right and all the rest of us wrong. All I have done here is calculate how spectacularly wrong we would be, if McIntosh is right.”
The effect of gradual change over an extremely long period of time certainly has to be the most underestimated effect of the theory of evolution. There wasn’t a “first” human because that is now how species evolve. The change is too gradual to perceive from moment to moment, just like the hour hand of a clock, as Professor Dawkins suggests. To further illustrate the point, let’s pretend it takes the hour hand a few million years to go from hour to hour, then you will get a sense of how long it takes to see significant change on an evolutionary timescale.
What is your first guess when thundering hoofs approach? Horse? Bison? From now on, mine is zebra. Catching the zebra means exhausting virtually all possible alternatives, and then finding one more. This oddly clad horse is neglected not because it is unworthy, but simply because it is uncommon. There’s no need to worry about it because it just doesn’t happen.
On August 18, I caught a zebra. Upon first examination, it apparently had the classical symptoms of a bothersome, albeit ultimately benign case of strep throat. My father a surgeon, my mother a nurse, we were composed about my condition and utterly secure in the prognosis. We perused WebMD (“just in case”), and sure enough, our suspicions were confirmed: “A sudden, severe sore throat,” “pain when you swallow,” “fever over 101°F (38.3°C),” “swollen tonsils and lymph nodes,” “white or yellow spots on the back of a bright red throat”; all of which I displayed. That was a relief; after a brief bout of antibiotics and decadent ice cream therapy, my truant health would return.
Not so fast. These swollen tonsils seemed exceptionally…well, swollen! I couldn’t eat; I couldn’t even sip some water. Something was wrong. I went to the doctor (you know, just in case), and sure enough, it wasn’t strep; it was that terrible sleeping giant that lurks in every college students’ subconscious: mono. Despite being guilty of its colloquial name, I knew the kissing disease couldn’t keep me down. How could it? I was the healthiest person I knew. I spent the majority of my summer days either exercising or consuming healthy food (with only the occasional toxin). They say mono drains your energy; good thing I had a perpetual surplus.
Okay, so I would need a few more days of recovery than I expected. Still, no big deal. I was resilient and would bounce back just in time to begin fall semester. I returned to WebMD just to confirm my diagnosis. The verdict: classic mono.
After a week of some good old-fashioned suffering thanks to vicious fevers and the concomitant sense of helplessness, my symptoms again failed to meet my expectations. “It says right there, seven to ten days. It’s been ten days.” Then again, everyone is different, so maybe my course would be different. For the first time, my suspicions were proven right.
A suspiciously intense pain hit my left abdomen, leaving me with a sudden loss of comfort that Jessica Biel could not have restored. I could no longer sit comfortably, my breaths reduced to pathetic wisps. I had to do something. I sat in the hospital waiting room, suffering through the longest half hour of my life.
The next few hours were a blur, streaming from my first ambulance ride, to checking into an empty hospital room, and finally ending in a bedside conference with the doctors’ first assessment: “this guy is really, really sick.” Fortunately, I had six outstanding specialists, and my chief doctor—reminiscent of Dr. House—was extremely thorough in the tests she ordered and even more shrewd in her correct conclusions. She recognized a unique Gram-negative Fusobacterium necrophorum that had invaded my bloodstream and established an internal jugular thrombus. The combination of her quick assessment and the radiologist’s recollection of this unusual disease, they delivered the final verdict: I had Lemierre’s Syndrome.
Lemierre’s Syndrome is quite rare; it occurs in approximately one in every million people in the general population. However, a recent review of the literature suggests that citations have been on the rise since 1990 (Riordan & Wilson, 2004). This review also mentions all of the symptoms I had experienced as the same ones that André Lemierre observed when he first discovered the disease in 1936:
The patients in this group were young, previously healthy, adolescents or young adults presenting with initial pharyngotonsillitis or peritonsillar abscess, often followed by swelling and tenderness along the sternomastoid muscle due to septic thrombophlebitis of the internal jugular vein. High fevers and rigors developed within a week and subsequently metastatic abscesses commonly to lung, bone, joints, and skin and soft tissues (Riordan & Wilson, 2004).
Of everything I endured from the inflamed tonsils, high fevers, rigors, pleurisy, and myriad other difficulties, my most salient memory of this whole experience is the profound sense of helplessness that I felt while lying in my bed facing my doctor. She looked at me with the soft eyes of a mother, but the determination of a warrior. This illness was palpably destroying my body—as shown in my chest X-Ray—and we both knew it. Until I got sick, I had done everything right, and yet everything had gone horribly wrong. Despite these ominous signs, I knew that I would be okay. I felt an immense trust in her: the kind reserved for the loving members of one’s immediate family. The words “doctor-patient relationship” fail to capture the depth of this connection, and this experience drives my resolution that if I do aspire to become a doctor, I’ll remember how a brilliant doctor once joked, “This is when it’s good to be a nerd.”
Lemierre’s Syndrome is extremely serious and potentially life threatening. The most misleading aspect of this disease is that the initial stages are ostensibly common—such as the typical onset of a sore throat and high fevers—but failure to act quickly can put the patient’s life in jeopardy. Early diagnosis is key to treatment, and any abnormal signs such as the rigors or others from the constellation of symptoms necessitate greater investigation.
So how do you get to Z without skipping the more plausible M (mono) or S (strep)? By remembering that zebras are still out there, and knowing when you’ve spotted one.
References
Riordan, T and Wilson, M (2004). Lemierre’s syndrome: more than a historical curiosa. Postgrad Med J; 80:328–334.
Recent research on belief formation in social groups suggests that “when just 10 percent of the population holds an unshakable belief, their belief will always be adopted by the majority of the society.”
Could this be the underlying cause for a few raving lunatics (Glenn Beck and Sarah Palin come to mind) getting so much press these days?
Dawkins Makes An Eye:
http://www.youtube.com/watch?v=lEKyqIJkuDQ
Here’s a pretty cool video (only about 2 min long) that speaks to one of the commonly cited examples of “irreducible complexity,” or less commonly known as the “I don’t know how else it would work” hypothesis.
After watching the video, it is actually very easy to imagine how the eye may have evolved. The key point here is that cells do not all of a sudden, randomly assemble into complex structures, as some people (who do not understand the fundamentals of evolution) would suggest. There are a series of very small, simple changes that could lead to the type of eye we now possess, and as evidence for this we can look around to see if there are any intermediate forms. Dawkins rightly points out that “…all those stages actually do exist, even within one class of animals, the molluscs.” That is how you test a hypothesis. We would expect to see certain forms based on evolutionary theory, and we do see a steady progression of intermediates. ID does not have falsifiable hypotheses, because their claims are not testable. In fact, that is kind of the whole point of calling them “designed”: we don’t understand how they work, so it must have been someone smarter who put them there.
There is not just one perfect eye that jumped out of nowhere. It has been improved over and over, little by little, over a long period of time. Even our eyes now are certainly not perfect. We have a blind spot that get’s “filled in” by our mind in normal vision (see link for blind spot tests you probably tried when you were a kid). We also have very restricted clarity in most of our field of view; scientists such as Mark Fairchild have discussed how our most acute vision—detected by the center of the retina at a spot called the fovea—is limited to about twice the size of a thumbnail held out at arms length.
Irreducible complexity is illusory; it is not scientific, and I don’t think there could actually be such a thing as an active ID scientist. It’s a good thing evolutionary scientists don’t throw up their hands and quit when they don’t understand something, otherwise we wouldn’t make new progress and new discoveries…kind of like the evidence for ID.
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