Oct 15 2011

Chocolate lovers: climate change affects you!

Every now and then something brings home what climate change could do to us: no chocolate!

Researchers in Colombia predict that the 1 degree rise in world temperatures expected by 2030 will hit small cocoa farmers in West Africa. particularly hard.  Farmers in Ghana and Cote d-Ivoire produce half the world’s cocoa.

The 2 degree rise expected by 2050 will make it impossible for them to grow the plants at current elevations.

Now that’s something to worry about over the weekend, no?

  • Anthro

    Will the farmers have time to adapt to growing cocoa in other parts of their countries? Is that a completely naive question?

    I realize there is much more at stake than cocoa for MY favorite confections, but….oh never mind, I could so easily maintain my weight if it weren’t for chocolate! But seriously, what will happen to all the displaced farmers? I am not so concerned about commodity traders that hoard the stuff.

  • http://wholemindblog.blogspot.com Kay Loughrey

    No chocolate would be a tragedy! A shortage of chocolate worldwide would be a wake up call worldwide. But by then it’s likely to be too late.

    So, what do is the most import thing you believe we do now to stem this chocolate catastrophe (not to mention that some of the world’s major seaports may be underwater by then)?

    Anything beyond eating less red meat and a more plant based diet that you recommend? Does buying locally really make a difference from your point of view?

    Kay Loughrey, RD
    Nutritionist

  • Michael

    Kay L:

    Individual lifestyle changes reduce individual impacts, but we need to move the entire global economy off of the fossil fuels that are driving the problem. Might I suggest it would be much more effective to donate to one of the many credible environmental organizations pushing for legislation to shift us to a clean energy nation, and then signing up for their letter-writing campaign alerts and committing to following up on at least one of them once a month?

  • Lysander

    The entire premise is flawed with the absurd assumption that temps
    “are expected” to rise at that precise rate. Why not consider the possibility that temps may decline at the same rate and what effect that may have on the cocoa growers?

  • Michael

    Lysander:

    Because temps /aren’t/ expected to decline. There is, as you’re probably aware, a very strong scientific consensus that human-derived greenhouse gasses, primarily from the burning of fossil fuels and from agricultural methane, are increasing global mean temperatures and disrupting climate systems today, with the trends continuing and worsening for the next century or more. The main question now is how much worse we will make it, based on whether we continue to burn fossil fuels according to a business-as-usual projection, or bring our use of them down by increasing energy efficiency and converting our economies over to non-greenhouse-gas-polluting energy sources.

  • Margeretrc

    @Lysander and @Michael, There is, indeed, a very strong scientific consensus that global temperatures are increasing and will continue to do so as a result of, at least in part and perhaps mostly, human activities. While a consensus doesn’t make it so (there’s also a consensus, though not as strong–there are those who disagree–that cholesterol causes heart disease and that isn’t so) this consensus is based on logic and a tremendous amount of scientific data. We do, indeed, need to “bring our use of [fossil fuels] down by increasing energy efficiency and converting our economies over to non-greenhouse-gas-polluting energy sources,” and not just so people can continue to grow cocoa. Though the loss of chocolate would, indeed, be a tragedy, there are consequences much worse than that and we’re already experiencing some of them.

  • Marie

    I guess no more child labor in cocoa farms then

  • Michael Bulger
  • Margeretrc

    @Michael, I’m well aware of what the “experts” say about cholesterol and heart disease. I am also a scientist who knows that correlation does not equal causation. Just because cholesterol is a risk factor for heart disease–and, by the way, loads of people who do not have high serum cholesterol get heart disease and die of heart attacks, just one of the many “black swans” disproving the whole “cholesterol causes heart disease” hypothesis–doesn’t by any stretch mean that it causes it. The association has to be consistent (it’s not) AND there needs to be a plausible mechanism by which cholesterol causes heart disease (there isn’t.) The current, more reasonable hypothesis is that inflammation and/or infection cause heart disease and cholesterol is only implicated because it is involved in healing artery walls that have been damaged by elevated blood sugar, PUFAs (Polyunsaturated Fatty Acids), and sundry other things by which we assault our artery walls. I could go on, but I would recommend reading “Fat and Cholesterol are Good for You” by Uffe Ravnskov and doing a little critical thinking. Ever wonder why a substance, cholesterol, which the body needs and uses in so many ways and has been with us since we became animals, could suddenly (over the last 4 or 5 decades) become harmful to us? And only if we are not Inuits or Masai or French? It simply does not make sense and the whole idea is based on a house of cards–a fraudulent study that cherry picked data from 7 countries even though data from 22 was available to show a link between saturated fat and heart disease where there is none. Here’s a link for you: http://www.thincs.org so you can become acquainted with doctors and scientists around the world who, for good reason, do not accept the idea that cholesterol causes heart disease.

  • Anthro

    Thank you Michael! I was trying to think of a good link for Margaret.
    ——-
    A scientific consensus does make it so. Odd theories from journalists and fake “nutritionists” who cherry pick studies do not. It is irresponsible to tell people that their cholesterol levels do not matter or that they can eat all the fat they wish if only it is a “good” fat. Fat is fat and too much makes you FAT along with any other excess calories you consume. Obesity (along with high cholesterol) is a risk factor for heart disease.

  • Margeretrc

    @Anthro, “A scientific consensus does make it so”? Luckily we (at least some of us) learned a long time ago (in Copernicus and Galileo’s time) that it’s the data and evidence that counts. “Odd theories from journalists and fake “nutritionists” who cherry pick studies do not. ” That’s pretty much what the Lipid Hypothesis that says cholesterol causes heart disease is! “It is irresponsible to tell people that their cholesterol levels do not matter or that they can eat all the fat they wish if only it is a “good” fat.” Cholesterol levels do matter, actually. I want mine as high as possible. Among people my age (65) high cholesterol is associated with longer life than low. What’s irresponsible is to tell people they need to take a drug with some serious side effects to beat down a substance which they’re brains, especially, and other parts of their bodies–including their immune system–need and to tell people they shouldn’t be eating the natural fat that they need to be healthy and that has been keeping humans healthy for 99+% of our existence. “Fat is fat and too much makes you FAT along with any other excess calories you consume.” Actually, there is fat (like trans fats and PUFAs) which we definitely should not be eating, and then there is fat (like olive oil, buter, lard (whose FA profile is very close to olive oil, BTW) and coconut and palm oil, all of which people have been eating without developing heart disease (and healthy people still do) for most of our existence. “Too much of anything will make you fat.” The beauty of natural fats is we are hard wired NOT to eat too much of it. It satisfies us and helps us know when to stop eating. Not so with carbohydrates, especially sugar and starchy grains, which would and do have us eating more and more, because we don’t know when to stop without artificial means like counting calories, etc. If you’re not eating enough fats, you are eating too many carbohydrates. “Obesity (along with high cholesterol) is a risk factor for heart disease.” Again, risk factor does not mean cause. How do you know that the same thing that causes obesity isn’t also causing heart disease? Many people who get heart disease are not obese and many who are obese do not have heart disease. Again, consistency is required and is not there. The idea that cholesterol causes heart disease should have died a long time ago for lack of evidence, except that there is a multi-billion dollar industry that depends on us believing what many scientists and doctors (as well as some qualified journalists and nutritionists who have done their research) do not. Sadly, many journalists and fake nutritionists do still buy into the idea and propagate it.

  • Margeretrc

    @Anthro and @Michael, Instead of telling me and giving me links to what the “consensus” says, why don’t you try giving me a scientific explanation for a) why people like the Inuits, the Masai, and the French, among others, who eat traditional diets high in saturated fat and cholesterol, do not have the sky high rates of heart disease and obesity that we see in this country and b) a plausible biological mechanism for how cholesterol causes heart disease (in only some people.)
    Oops: “they’re brains” I meant “their brains”
    And “Too much of anything will make you fat” should not be in quotes. You did not say that, Anthro, I did.
    BTW, the evidence/data do support both anthropogenic global warming and evolution. I totally accept that those ideas are grounded in science. If/when the evidence that cholesterol causes heart disease becomes conclusive–and consistent–and a plausible mechanism for how it does is proposed, I will accept that, too, but for now there are too many “black swans” and no plausible biological mechanism.

  • Michael Bulger

    Okay, Margaret. The Masai are very physically active (they walk everywhere). Their life expectancy is short (under 50 according to BBC), lessening the chance that their mortality is a result of heart disease. They actually develop thickening by atherosclerosis at a very high level, but they are so active that their coronary vessels enlarge remarkably, as a result of their extremely physical lifestyle. (http://aje.oxfordjournals.org/content/95/1/26.abstract)

    The Inuit traditionally eat seal meat, which more closely resembles fish meat by being high in “Highly Unsaturated Fatty Acids”/PUFA (http://pubs.acs.org/doi/abs/10.1021/bk-1994-0558.ch016). Seal meat does not equate to butter, beef, or bacon. The Inuit also have shorter life expectancies than the average North American, lessening their chance of developing heart disease due to cholesterol accumulation.

    The French traditionally eat small portions and plenty of veggies, fruits, and breads. They are also more active than the Americans. However, they too are experiencing a rise in obesity and related diseases as their habits become more similar to Americans. Part of the discrepancy has been explained in how cause of death was listed by French doctors and the “time lag” in dietary choices (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115846/).

    As for “b)”, I’ll simply quote NIH: “When there is too much cholesterol (a fat-like substance) in your blood, it builds up in the walls of your arteries. Over time, this buildup causes “hardening of the arteries” so that arteries become narrowed and blood flow to the heart is slowed down or blocked. The blood carries oxygen to the heart, and if enough blood and oxygen cannot reach your heart, you may suffer chest pain. If the blood supply to a portion of the heart is completely cut off by a blockage, the result is a heart attack.”

    There are many factors that go into heart disease. That is sufficient to explain why the presence of one-risk factor in an elevated level does not consistently result in a negative health outcome. Another example of this principle is that many who people smoke tobacco and have the lungs of a smoker do not die from lung cancer.

  • Michael Bulger

    Another example of this principle is that many *people who* smoke tobacco and have the lungs of a smoker do not die from lung cancer.

  • MargaretRC

    Seriously? You are comparing tobacco smoke to cholesterol? Yes, a small percentage of people who smoke get away with it. But a) the link between smoking and lung cancer is considerably stronger than that between cholesterol and heart disease and b) there is a very plausible mechanism for tobacco smoke causing disease when it does and c) we don’t need to smoke. It’s a foreign substance entering our bodies! That’s entirely different. Cholesterol is a substance our bodies need and are capable of making (unless we
    stop it with drugs) if we don’t consume enough for its needs. It’s been coursing through our arteries and veins (packaged in lipoproteins) for as long as we’ve been around as a species and is, in fact, key to all animals. It’s a key component of our cell membranes, nerves, and more for equally as long. The rise in the incidence of heart disease is a fairly recent event and unlikely to be caused by something that’s been with us forever!

  • Michael Bulger

    There are many, many things that have long existed in our environment and that our body naturally produces that are problematic in excess.

    I offered a plausible mechanism:

    “When there is too much cholesterol (a fat-like substance) in your blood, it builds up in the walls of your arteries. Over time, this buildup causes “hardening of the arteries” so that arteries become narrowed and blood flow to the heart is slowed down or blocked. The blood carries oxygen to the heart, and if enough blood and oxygen cannot reach your heart, you may suffer chest pain. If the blood supply to a portion of the heart is completely cut off by a blockage, the result is a heart attack.”

    Try visiting this page: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004449/#adam_007115.disease.causes

  • Margeretrc

    “Fatty material and other substances form a plaque build-up on the walls of your coronary arteries. The coronary arteries bring blood and oxygen to your heart.” No one, including myself, is disputing that this is what happens. What I and many others dispute is just what that “fatty material” is. “When there is too much cholesterol (a fat-like substance) in your blood, it builds up in the walls of your arteries.” What is “too much?” As I said, heart attacks aren’t limited to people who have “high” cholesterol, whatever that is. “Extra cholesterol in your blood builds up inside the walls of your heart’s arteries (blood vessels).” If that’s true, why is that just as many people with low cholesterol get heart disease and have heart attacks as have moderately high (high 200s)?. Heart disease and MIs only become more frequent among the small percentage of the population that have truly high (over 300) cholesterol–the ones who have Familial Hypercholesterolemia. They have a genetic defect in the mechanism that removes LDL cholesterol from the blood stream, but among even them there are those who live a long, disease free life! Check the actual data from the myriad studies that have tried to prove–without success–that cholesterol causes heart disease. (Uffe Ravnskov, M.D.–yes, he’s a doctor–does a great job of going through all the data in “Fat and Cholesterol are Good for You.” He also offers an alternative hypothesis–that is more reasonable and fits the data better–as to what causes that build up of plaque and heart disease.) Cholesterol doesn’t just float around free in the blood stream so it can stick to the artery walls. And cholesterol is a fatty substance–not sticky in its natural state. And why only artery walls? And why only certain artery walls–mostly the coronary arteries? Veins don’t build up plaque. Also, cholesterol is not the only thing found in the plaque build ups that lead to heart attacks. Poly unsaturated fatty acids and white blood cells are also found there. And the cholesterol found is oxidized. These are all questions and facts that need to be explained by any hypothesis about the cause of heart disease and the lipid hypothesis that cholesterol causes heart disease doesn’t. The difference between you and me, Michael, is that, while I, too, am very familiar with all the usual arguments and literature and, like you, I even believed them at one time, I have moved on. I have read a lot of literature, both on line and in print, by qualified critical thinkers that question the “conventional wisdom” and make infinitely more sense. In addition to Uffe Ravnskov’s book, there is “Know Your Fats” by Mary Enig, PhD., “Protein Power” by Drs. Michael and Mary Dan Eades, and “Good Calories, Bad Calories” by Gary Taubes. There is also “What if it’s all a big fat lie?” in The New York Times a bunch of years ago and “The Soft Science of Dietary Fat” in “Science”, both by Gary Taubes. There is a lot more, if you care to look.

  • Michael Bulger

    I’m familiar with the argument, counter-argument, and counter-counter-argument. Its your choice to “move-on”. When you’re advocating for an opinion that runs counter to established scientific consensus on how to save lives, you should expect to be contradicted.

  • Margeretrc

    “When you’re advocating for an opinion that runs counter to established scientific consensus on how to save lives, you should expect to be contradicted.” Fair enough. But I haven’t advocated for an opinion so much as suggested that the “established scientific consensus” needs to be re-examined as it has its origins in a faulty study, there is much that it does not explain, and there are serious questions as to whether or not it actually does save lives. It’s an “established scientific consensus” that many scientists do not agree with, which brings into question just how much of a consensus it is. Mainstream? Yes. Established? Yes. Consensus? Not so much. In science, one can never prove a hypothesis, just collect data in support. On the other hand, in science it only takes one set of contradictory data to disprove a hypothesis. As I’ve tried to show, a great deal of such contradictory data exists (that’s not an opinion, or an argument, it’s a statement of fact) that should call the lipid hypothesis (that cholesterol causes heart disease) into question. Believe what you want. I choose to go with what the science says, even if it’s not mainstream or established. It’s just a shame that the lipid hypothesis refuses to die, because that means mainstream medicine isn’t even looking for alternative causes or cures for a very serious disease that still kills a lot of people.

  • Michael

    Margeretrc:

    I’m sorry now to have to disagree with your reading of these cross-cultural comparisons (never a good source of evidence — too many confounding variables) and their implications for the strongly evidence-backed consensus view that high intake of saturated fat, and high levels of LDL cholesterol (especially, but not exclusively, in the presence of low HDL) are the major players in atherosclerosis.

    The Inuit haven’t historically had much atherosclerosis because they are extremely physically active, burning off a lot of their fat intake and causing a large shift of their cholesterol into HDL, and also because their life expectancies have been so short.

    It’s a myth that the Masai don’t have much atherosclerosis: autopsy studies in fact show that “Measurements of the aorta showed extensive atherosclerosis with lipid infiltration and fibrous changes but very few complicated lesions. The coronary arteries showed intimal thickening by atherosclerosis which equaled that of old U.S. men.” (“Atherosclerosis in the Masai,” George V. Mann, Anne Spoerry, Margarete Gary, And Debra Jarashow, American Journal of Epidemiology, 95(1): 26-37).

    The French haven’t historically had much atherosclerosis because of a mixture of an artifact of historical lag and small portion sizes: despite what we experience in French restaurants, the *absolute* intake of saturated fat by the French was for many decades not remarkable, and their worsening habits (including rising saturated fat intake) over time have caught up with them:

    http://www.bmj.com/content/318/7196/1471.extract

  • Margeretrc

    Michael, If I based my skepticism of the consensus view only on cross cultural comparisons, you might have a point, but I don’t. However, I will address those points first. The Masai do have atherosclerosis–one explanation is that we all get it over time because we all suffer some damage to our arteries that needs to be repaired and cholesterol is both the repairman and a necessary lubricant for those regions of our circulatory system most subject to stress–but they rarely have heart attacks (at least the ones who follow a traditional diet.) As to the Inuits, sure exercise is important, but can you say for sure that that is the only factor that protects them? That if they weren’t active, all that fat and cholesterol would kill them? Based on what? Also, I didn’t say that LDL has nothing to do with it, I said cholesterol isn’t the cause of heart disease. LDL isn’t cholesterol. It contains cholesterol, yes, but the kind of LDL found in atheromas also contain PUFA. LDL–in particular, oxidized LDL, is definitely involved, but is it the cholesterol that initiates the process? Or is the initiator the PUFA in the LDL membrane, which are highly susceptible to oxidation and which, in turn, oxidize the cholesterol, which is an antioxidant? I believe it’s the PUFA, and I base that not just on the epidemiological evidence that heart disease and heart attacks have been increasing steadily since we were all told to substitute poly unsaturated fats for saturated fats in our diet. I also base it on extensive research into the biochemistry of dietary fats. True, the French exercise portion control, but they do because they include plenty of fat, including sat. fat, in their food. Those of us who aren’t afraid of fat, including sat. fat, also exercise portion control naturally, without feeling hungry or counting calories. (And by including saturated fat in our diets, reducing proportionately the starchy carbohydrates and sugar, we increase our HDL, increase our large, fluffy, protective LDL, and decrease our triglycerides and small, dense, dangerous LDL–all factors which reduce our risk for heart disease.) No, I base my skepticism also on the fact that few, if any of the RCT and observational studies that have tried to link dietary intake of saturated fat and cholesterol to heart disease have failed to do so, including the famous Framingham study, and the fact that cholesterol is a substance which is pervasive in its presence and use in the human body and has been with us since long before the relatively recent rise in heart disease. Why would a substance that we need and use in so many ways–that is vital to our survival–suddenly turn deadly about 40 or so years ago? We didn’t start eating more (saturated fat and) cholesterol 40 years ago. In fact, we started eating less because we were led to believe it’s harmful, and continue to do so. Yet the rate of heart disease continues to climb!!!! Clearly something is wrong with the conventional wisdom. Here is just one discussion of experimental evidence that exonerates cholesterol: http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html

  • Michael Bulger

    A few points Margaret:

    Many strong studies show that replacing SFA with PUFA reduces heart disease.

    Cholesterol intake wasn’t measured 40 years ago.

    Saturated fat consumption might be down comparatively, but it is still well over recommended levels.

    Hardly anyone follows the Dietary Guidelines, so what we are told to eat does not always correlate with health.

  • Margeretrc

    “Many strong studies show that replacing SFA with PUFA reduces heart disease.” Such as? If that’s the case, it’s a mystery to me why heart disease has gone up as PUFA consumption has increased and and sat. fat consumption has gone down. Regardless of what you say about people not always following the guidelines, the record shows that sat. fat consumption has gone down, PUFA consumption has gone up and heart disease continues to rise. Mind you, I think over consumption of PUFA at the espense of sat. fat is a only contributing factor to heart disease, not necessarily a cause. I think many things contribute to heart disease. Natural cholesterol just isn’t one of them, and neither is saturated fat. Fear of sat. fat and cholesterol, however, have unequivocally resulted in over consumption of sugar and other starchy carbohydrates and that is leading to many unintended and unfortunate consequences for the health of people in the western world.

    “Cholesterol intake wasn’t measured 40 years ago.” So? Being able to measure something makes it somehow deadly? Even Ancel Keys, father of the Lipid Hypothesis said it would be ridiculous to conclude that dietary cholesterol has any effect on serum cholesterol.
    “Hardly anyone follows the Dietary Guidelines, so what we are told to eat does not always correlate with health.” It correlated with my personal health. I followed the guidelines and got fat and unhealthy. I stopped following the guidelines and lost the weight and got healthy. That’s an n=1 experiment and not valid, I know, but it’s all I need to know for myself and it definitely shows that, at least for one person, the guidelines were totally wrong. I also know I am far from the only one. Ever consider that some of the healthiest people are NOT following the guidelines? No, I don’t suppose you do.

  • Margeretrc

    I suspect we’re done, but in case we’re not: http://www.dietdoctor.com/saturated-fat-nothing-to-worry-about
    You can download the whole study, published in the Netherlands Journal of Medicine, as a PDF or just read the abstract, nicely supplied in the comments by @moreporkplease. It seems if/when PUFA are protective against CVD, it’s the omega-3, not the omega-6. Makes sense to me.