# What causes heart attacks? **URL:** \ **Category:** Factual Questions\ **Created:** [July 28, 2010, 2:38am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259 "2010-07-28T02:38:42Z")\ **Posts on this page:** 12\ **Page:** 4
**Author:** ![Grateful-UnDead](https://avatars.discourse-cdn.com/v4/letter/g/ccd318/32.png) [@Grateful-UnDead](https://boards.straightdope.com/u/Grateful-UnDead)\ **Post date:** [August 9, 2010, 8:24am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/61 "2010-08-09T08:24:00Z")
> [@needscoffee](#): > > > [@Grateful-UnDead](#): > > > > Over the weekend, I read both the papers by Warburton et al and Mente et al, referred to in posts above. > > > > Both make fascinating reading, particularly since they seem to suggest that many of the public health assertions we are bombarded with are apparently in contradiction to the empirical evidence. > > > > This got me to thinking about other related issues: specifically, > > > > What is the evidence regarding salt? Is it really the poison of the Devil? Or is it a victim of misinformation? > > > > How about “fast food” and “junk food”. Are they just victims of bad press, or is there really some scientific basis for their pariah status? > > All of this is covered in **Good Calories, Bad Calories**. Taubes has something like 100 pages of end notes referencing studies he re-evaluated. Basically, salt = victim of misinformation; carbs are the problem. Carbs cause insulin and insulin-related growth factor to be released, both of which seem to be driving most of the problems in metabolic syndrome, as well as growth of tumors which are estrogen-dependent, such as breast and colon cancers, whose tumors have far more insulin receptors than ordinary tissue. I am still waiting for my copy of “GCBC”, so in the absence of that source, let me direct the questions to you. What happened to salt; how is it that it has become the “victim of misinformation”. How did this come about, and what is the “real story”? What is “metabolic syndrome”? Is the contention that the ailments you cite as being carbohydrate/insulin driven, the reason “junk food” and “fast food” are seen as being the epitome of evil? ---
**Author:** ![needscoffee](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/needscoffee/32/1076_2.png) [@needscoffee](https://boards.straightdope.com/u/needscoffee)\ **Post date:** [August 10, 2010, 6:47am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/62 "2010-08-10T06:47:50Z")
[Metabolic Syndrome](http://www.nlm.nih.gov/medlineplus/metabolicsyndrome.html) > [@](#): > > \*\*Metabolic Syndrome \*\* > > ``` > URL of this page: http://www.nlm.nih.gov/medlineplus/metabolicsyndrome.html > > Also called: Insulin resistance syndrome, Metabolic Syndrome X > > > Metabolic syndrome is a group of conditions that put you at risk for [heart disease](http://www.nlm.nih.gov/medlineplus/heartdiseases.html) and [diabetes](http://www.nlm.nih.gov/medlineplus/diabetes.html). These conditions are > > ``` > > [ul] > [li] [High blood pressure](http://www.nlm.nih.gov/medlineplus/highbloodpressure.html)[/li][li] High blood sugar levels[/li][li] High levels of [triglycerides](http://www.nlm.nih.gov/medlineplus/triglycerides.html), a type of fat, in your blood[/li][li] Low levels of HDL, the good [cholesterol](http://www.nlm.nih.gov/medlineplus/cholesterol.html), in your blood[/li][li] Too much fat around your waist[/li][/ul] > [@](#): > > Is the contention that the ailments you cite as being carbohydrate/insulin driven, the reason “junk food” and “fast food” are seen as being the epitome of evil? Yes. Taubes gives numerous cites of isolated populations who eat high fat/protein diets with no carbs who have no incidence of any of the metabolic syndrome conditions, who when carbs are introduced to their diets quickly develop them. Not only heart disease, but the estrogen-dependent cancers, acne (hormonally based as well), and probably more that I’m forgetting. Upthread I linked to a video lecture Taubes gave. It has a lot of good information, although its focus is more on overweight issues. I can’t remember specifics of how salt came to be considered dangerous, but it’s in the book. He does go into it pretty extensively. ---
**Author:** ![Grateful-UnDead](https://avatars.discourse-cdn.com/v4/letter/g/ccd318/32.png) [@Grateful-UnDead](https://boards.straightdope.com/u/Grateful-UnDead)\ **Post date:** [August 11, 2010, 12:29am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/63 "2010-08-11T00:29:36Z")
Thanks for the responses; I will follow up on your links. Where is that darn book!!! Should have ordered through Amazon!!! However, to go off topic a bit: I read in this morning’s newspaper that a study has just been published that reveals that girls are entering puberty at an ever decreasing age. Apparently puberty has been detected in girls as young as 5. In the posts above, there is repeated reference to the link between carbohydrates in the diet and estrogen dependent cancers. Is it too much of a stretch to suggest that carbohydrates are a causative factor in this observed early onset puberty? If so, what would be the link between carbohydrates and estrogen synthesis? I am speculating here that early puberty is due to the premature production of estrogen. ---
**Author:** ![needscoffee](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/needscoffee/32/1076_2.png) [@needscoffee](https://boards.straightdope.com/u/needscoffee)\ **Post date:** [August 11, 2010, 2:03am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/64 "2010-08-11T02:03:36Z")
There are so many possible factors that could contribute to early onset puberty. This certainly seems like it could play a role. I don’t recall if this was mentioned in the book or not, but after you read it, you could send Taubes an email and see if he’s considered it. I emailed him with a question about a nutrition study described on NPR which seemed to be contradictory to other studies, and he sent back a very long, in-depth response the same day explaining the study and its background. I was very impressed. ---
**Author:** ![KarlGauss](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/karlgauss/32/3713_2.png) [@KarlGauss](https://boards.straightdope.com/u/KarlGauss)\ **Post date:** [August 11, 2010, 2:09am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/65 "2010-08-11T02:09:27Z")
> [@Grateful-UnDead](#): > > . . . what would be the link between carbohydrates and estrogen synthesis? . . . Just my opinion, but excess carbs may promote both obesity and insulin resistance, with real potential for a vicious cycle (obesity leading to more insulin resistance, and insulin resistance leading to more obesity). Since fat tissue is a source of estrogen, it’s not surprising, therefore, that obese, insulin resistant people have generally higher estrogen levels. ---
**Author:** ![Grateful-UnDead](https://avatars.discourse-cdn.com/v4/letter/g/ccd318/32.png) [@Grateful-UnDead](https://boards.straightdope.com/u/Grateful-UnDead)\ **Post date:** [August 11, 2010, 3:20am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/66 "2010-08-11T03:20:26Z")
> [@KarlGauss](#): > > > [@Grateful-UnDead](#): > > > > . . . what would be the link between carbohydrates and estrogen synthesis? . . . > > Just my opinion, but excess carbs may promote both obesity and insulin resistance, with real potential for a vicious cycle (obesity leading to more insulin resistance, and insulin resistance leading to more obesity). Since fat tissue is a source of estrogen, it’s not surprising, therefore, that obese, insulin resistant people have generally higher estrogen levels. Is fat tissue a repository of estrogen, which was produced elsewhere; or is it directly involved in its synthesis? Ie: does more fat = more estrogen? In the case of early onset puberty, would the logic be: high carbohydrate intake =\> higher body fat =\>excess production of estrogen ? Or would it be excess carbohydrate =\> unknown mechanism =\> early production of estrogen =\> accumulation of estrogen in body fat =\> early onset of puberty? So would loss of body fat delay early onset of puberty? ---
**Author:** ![KarlGauss](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/karlgauss/32/3713_2.png) [@KarlGauss](https://boards.straightdope.com/u/KarlGauss)\ **Post date:** [August 11, 2010, 9:40am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/67 "2010-08-11T09:40:47Z")
> [@Grateful-UnDead](#): > > > [@KarlGauss](#): > > > > Just my opinion, but excess carbs may promote both obesity and insulin resistance, with real potential for a vicious cycle (obesity leading to more insulin resistance, and insulin resistance leading to more obesity). Since fat tissue is a source of estrogen, it’s not surprising, therefore, that obese, insulin resistant people have generally higher estrogen levels. > > Is fat tissue a repository of estrogen, which was produced elsewhere; or is it directly involved in its synthesis? Ie: does more fat = more estrogen? Actually, fat tissue _is_ directly involved in the synthesis of estrogen. Basically, fat tissue possesses the enzymatic machinery (i.e. [aromatase](http://en.wikipedia.org/wiki/Aromatase)) to convert androgens (male hormone) into estrogen (i.e. estradiol) ([cite](http://en.wikipedia.org/wiki/Estradiol#Production)). As a result, it is the case that “more fat = more estrogen” just as you wondered. This fact has some real world implications. For example, obese women (who, as a result of fat tissue’s ability to make estrogen, have generally higher estrogen levels than non-obese women) have higher rates of estrogen-dependent cancers such as uterine cancer (i.e. endometrial Ca) and breast cancer. The effect of the high levels of estrogen in obese women also helps to explain why obese women are less likely to get osteoporosis (remember that estrogen deficiency, as occurs with menopause, is a major risk factor for osteoporosis). Obese men are also affected by the high levels of estrogen being produced by their fat tissue. For example, obese men often get breast enlargement ([gynecomastia](http://en.wikipedia.org/wiki/Gynecomastia)) which is a direct consequence of having too much estrogen. ---
**Author:** ![Grateful-UnDead](https://avatars.discourse-cdn.com/v4/letter/g/ccd318/32.png) [@Grateful-UnDead](https://boards.straightdope.com/u/Grateful-UnDead)\ **Post date:** [August 12, 2010, 2:13am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/68 "2010-08-12T02:13:22Z")
> [@KarlGauss](#): > > > [@Grateful-UnDead](#): > > > > Is fat tissue a repository of estrogen, which was produced elsewhere; or is it directly involved in its synthesis? Ie: does more fat = more estrogen? > > Actually, fat tissue _is_ directly involved in the synthesis of estrogen. Basically, fat tissue possesses the enzymatic machinery (i.e. [aromatase](http://en.wikipedia.org/wiki/Aromatase)) to convert androgens (male hormone) into estrogen (i.e. estradiol) ([cite](http://en.wikipedia.org/wiki/Estradiol#Production)). As a result, it is the case that “more fat = more estrogen” just as you wondered. > > This fact has some real world implications. For example, obese women (who, as a result of fat tissue’s ability to make estrogen, have generally higher estrogen levels than non-obese women) have higher rates of estrogen-dependent cancers such as uterine cancer (i.e. endometrial Ca) and breast cancer. The effect of the high levels of estrogen in obese women also helps to explain why obese women are less likely to get osteoporosis (remember that estrogen deficiency, as occurs with menopause, is a major risk factor for osteoporosis). Obese men are also affected by the high levels of estrogen being produced by their fat tissue. For example, obese men often get breast enlargement ([gynecomastia](http://en.wikipedia.org/wiki/Gynecomastia)) which is a direct consequence of having too much estrogen. Just thinking out loud here… If an obese woman develops pathological conditions as a result of the high levels of estrogen, doesn’t that imply that she had too high levels of androgen in the first place? Could there be a cause and effect relationship between her being obese and an excess of androgen? Ie: the body has too much androgen, so builds up fat; the fat absorbs the androgen and converts it to estrogen. Thinking along those lines, could the other pathological conditions that are associated with obesity, also be androgen related? Going even further, wouldn’t eating carbohydrates be a form of treatment for androgen related conditions? (Crude, but given the ling of thinking above, maybe it would work.) This could be confirmed when an obese woman loses weight; does she develop androgen related conditions? Still waiting for my copy of Taubes …! ---
**Author:** ![Alpine](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/alpine/32/17813_2.png) [@Alpine](https://boards.straightdope.com/u/Alpine)\ **Post date:** [August 13, 2010, 11:55pm UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/69 "2010-08-13T23:55:47Z")
Thanks to this thread, I downloaded and started reading Taubes’ book on my Kindle. Boy do I feel ignorant about nutrition and body chemistry! I guess I haven’t been paying attention, as I put the low-carb/no sugar movement down to yet another fad diet (which it also is, IMO). I’ve only read the first two parts of the book and am in the midst of the LDL discussion, but what I’ve read so far is enlightening. I’m not a conspiracy theory fan, and I like that Taubes doesn’t try to make out that the proponents of low-fat/AHA approved diets are all evil and secretly taking handouts from X industry, etc. Thanks, all, for bringing this to my attention. Makes a nice change from PG Wodehouse novels, and I’ll be planning some changes in my diet as well as in my assumptions. ---
**Author:** ![Grateful-UnDead](https://avatars.discourse-cdn.com/v4/letter/g/ccd318/32.png) [@Grateful-UnDead](https://boards.straightdope.com/u/Grateful-UnDead)\ **Post date:** [August 15, 2010, 3:01am UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/70 "2010-08-15T03:01:51Z")
> [@Alpine](#): > > Thanks to this thread, I downloaded and started reading Taubes’ book on my Kindle. Boy do I feel ignorant about nutrition and body chemistry! I guess I haven’t been paying attention, as I put the low-carb/no sugar movement down to yet another fad diet (which it also is, IMO). > > I’ve only read the first two parts of the book and am in the midst of the LDL discussion, but what I’ve read so far is enlightening. I’m not a conspiracy theory fan, and I like that Taubes doesn’t try to make out that the proponents of low-fat/AHA approved diets are all evil and secretly taking handouts from X industry, etc. > > Thanks, all, for bringing this to my attention. Makes a nice change from PG Wodehouse novels, and I’ll be planning some changes in my diet as well as in my assumptions. At least you are finding out the easy way! Imagine what it is like to wake up in a room that looks like the bridge on the Starship Enterprise, have both arms hooked up to all kinds bottles and drips, and then have a guy who looks like “The Angel Of Death” tell you that all the “right things” you have been doing and thinking, are completely irrelevant. Yesterday I received my copy of Taubes and have read the first 100 pages. Beyond the obvious eye openers regarding the “science” of health and nutrition, I am particularly taken by the huge part politics and ambition seem to play in this. This leads me to wonder how much else of what we are being told regarding health is just the furtherance of ambition and the pursuit of glory on the part of the proponents, as opposed to being objective science. I have about 500 pages of Taubes to go; is this going to be depressing or what! ---
**Author:** ![Surreal](https://avatars.discourse-cdn.com/v4/letter/s/eada6e/32.png) [@Surreal](https://boards.straightdope.com/u/Surreal)\ **Post date:** [March 14, 2011, 7:08pm UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/71 "2011-03-14T19:08:01Z")
Here’s another recent study linking marathon running to cardiovascular problems: > **[Diverse patterns of myocardial fibrosis in lifelong, veteran endurance...](https://pubmed.ncbi.nlm.nih.gov/21330616/)** > > This study examined the cardiac structure and function of a unique cohort of documented lifelong, competitive endurance veteran athletes (\>50 yr). Twelve lifelong veteran male endurance athletes \[mean ± SD (range) age: 56 ± 6 yr (50-67)\], 20... > [@](#): > > Aims - This study examined the cardiac structure and function of a unique cohort of documented life-long, competitive endurance veteran athletes (\> 50 years). Methods and Results - Twelve lifelong veteran male endurance athletes (mean ± SD [range] age: 56 ± 6 yr [50-67]), 20 age-matched veteran controls (60 ± 5 y; [52 - 69]) and 17 younger male endurance athletes (31 ± 5 years [26-40]) without significant co-morbidities underwent cardiac magnetic resonance (CMR) imaging to assess cardiac morphology and function, with CMR imaging with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Results - Lifelong veteran athletes had smaller LV and RV end-diastolic and end-systolic volumes (p\<0.05) but maintained LV and RV systolic function compared to young athletes. However, veteran athletes had a significantly larger absolute and indexed LV and RV end-diastolic and systolic volumes, intra-ventricular septum thickness during diastole, posterior wall thickness during diastole, and LV and RV stroke volumes (p\<0.05), together with significantly reduced LV and RV ejection fractions (p\<0.05) compared to veteran controls. **In 6 (50%) of the veteran athletes LGE of CMR indicated the presence of myocardial fibrosis (4 veteran athletes with LGE of non-specific cause, 1 probable previous myocarditis and 1 probable previous silent myocardial infarction). There was no LGE in the veteran controls or young athletes. The prevalence of LGE in veteran athletes was not associated with age, height, weight or BSA (p\>0.05), but was significantly associated with the number of years spent training (p\<0.001), number of competitive marathons (p\<0.001) and ultra-endurance (\>50 miles) marathons (p\<0.007) completed**. Conclusion - **An unexpectedly high prevalence (50%) of myocardial fibrosis was observed in healthy, asymptomatic life-long veteran male athletes, compared to zero cases in age-matched veteran controls and young athletes. This data suggests a link between life-long endurance exercise and myocardial fibrosis that requires further investigation** ---
**Author:** ![Surreal](https://avatars.discourse-cdn.com/v4/letter/s/eada6e/32.png) [@Surreal](https://boards.straightdope.com/u/Surreal)\ **Post date:** [March 14, 2011, 7:32pm UTC](https://boards.straightdope.com/t/what-causes-heart-attacks/548259/72 "2011-03-14T19:32:56Z")
Here’s a study in rats where the researchers were able induce VT simply by having them perform lots of strenuous exercise: [http://circ.ahajournals.org/cgi/content/short/123/1/13](http://circ.ahajournals.org/cgi/content/short/123/1/13) > [@](#): > > Male Wistar rats were conditioned to run vigorously for 4, 8, and 16 weeks; time-matched sedentary rats served as controls. Serial echocardiograms and in vivo electrophysiological studies at 16 weeks were obtained in both groups. After euthanasia, ventricular collagen deposition was quantified by histological and biochemical studies, and messenger RNA and protein expression of transforming growth factor-β1, fibronectin-1, matrix metalloproteinase-2, tissue inhibitor of metalloproteinase-1, procollagen-I, and procollagen-III was evaluated in all 4 cardiac chambers. \*\*At 16 weeks, exercise rats developed eccentric hypertrophy and diastolic dysfunction, together with atrial dilation. In addition, collagen deposition in the right ventricle and messenger RNA and protein expression of fibrosis markers in both atria and right ventricle were significantly greater in exercise than in sedentary rats at 16 weeks. Ventricular tachycardia could be induced in 5 of 12 exercise rats (42%) and only 1 of 16 sedentary rats (6%; P=0.05). The fibrotic changes caused by 16 weeks of intensive exercise were reversed after an 8-week exercise cessation. \*\* [Previous page](https://boards.straightdope.com/t/what-causes-heart-attacks/548259.md?page=3)