Oxidized Cholesterol 27HC May Explain 3 Breast Cancer Mysteries

Oxidized Cholesterol 27HC May Explain 3 Breast Cancer Mysteries
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Oxidized cholesterol (concentrated in products containing eggs, processed meat, and parmesan cheese) has cancer-fueling estrogenic effects on human breast cancer.

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

In 1908, the presence of cholesterol crystals was noted “in the proliferating areas of cancers,” suggesting that perhaps cholesterol, in some way, was “associated with the regulation of [cancer] proliferation.” A century later, we now recognize “the accumulation of cholesterol [as] a general feature of cancer tissue, and recent evidence suggests that cholesterol [may indeed play] critical roles in the progression of cancers, including breast, prostate, and colorectal cancers.”

Perhaps that could explain why “egg consumption was associated with increased breast cancer risk.” And, indeed, a systematic review of the evidence suggests that “dietary cholesterol intake increases risk of breast cancer,” and the more cholesterol you eat, the higher the risk appears to go. But, why?

One thought is that the “[p]rolonged ingestion of a cholesterol-enriched diet induces chronic, auto-inflammatory responses,” and we know that “chronic…inflammation can lead to the initiation, promotion, and progression of tumor development.” It’s true that sprinkling some cholesterol on white blood cells in a test tube can trigger the release of inflammatory compounds, and LDL cholesterol can induce breast cancer proliferation and invasion. But again, that’s in vitro, where you can show that like breast cancer cells can migrate nearly twice as far within a day in a petri dish in the presence of LDL cholesterol. But what about in people?

Well, the level of LDL cholesterol in the blood of women diagnosed with breast cancer does appear to be “a predictive factor of breast tumor progression.” About two years after surgery/chemo/radiation, not one of the women in the lowest third of LDL cholesterol levels had a cancer recurrence. The same could not be said for women with higher cholesterol. We know cholesterol can cause inflammation in our artery walls; maybe it’s also playing an effect on breast cancer initiation and progression? They speculate that the high cholesterol levels may have a “cancer-fueling effect.” And indeed, women with breast cancer who happen to be taking cholesterol-lowering statin drugs appear to live about 40 percent longer before the cancer comes back. But the data isn’t good enough to ensure the drug benefits outweigh the risks, though lowering cholesterol with diet, one may be able to get the best of both worlds. But what does this have to do with dietary cholesterol?

Sure, animal studies show that if you feed mice cholesterol, you can accelerate their cancers, “but extrapolation to humans is difficult as dietary cholesterol has limited effects on blood cholesterol levels in humans.” Thus, “dietary cholesterol might [just] be indicative of a lifestyle prone to health-related problems, including cancer.” Maybe people are just more likely to chase bacon and eggs down with a cigarette, compared to oatmeal? It’s hard to imagine how dietary cholesterol alone could promote cancer development. But that all changed recently, with the discovery that 27-Hydroxycholesterol, a metabolite of cholesterol, “can function as an estrogen and increase the proliferation” of most breast cancer cells.

Ah, so it’s not the cholesterol itself, but what it turns into in the body.Scientists have long struggled to understand why women with heart disease risk factors are more likely to develop breast cancer.” Now, perhaps we know. “The discovery that the most abundant oxidized cholesterol metabolite” in our bloodstream can have estrogenic effects may explain the link between high cholesterol and the development and progression of breast cancer and prostate cancer. Yes, 27-Hydroxycholesterol also stimulates the proliferation of prostate cancer cells, boosting growth by about 50 percent.

I’ve explored before the role oxycholesterols may play in mediating pro-oxidative and pro-inflammatory processes in degenerative diseases, such as Alzheimer’s and heart disease, but now it looks like oxidized cholesterol can play a role in all three stages of tumor development as well: initiation, promotion, and then the progression of cancer. Not just promoting the growth of breast cancer cells, but also inducing their invasion and migration—potentially facilitating breast cancer metastasis through suppressing anti-cancer immunity, and then inducing angiogenesis, helping breast tumors hook up their blood supply.

This is all supported by “several lines of evidence [that point to] a pathologic role” for this cholesterol metabolite. Yeah, you can feed mice cholesterol; their oxysterol levels go up and their tumors accelerate. It “also appears to dramatically hasten the spread, or metastasis, of breast tumors to other organs.” But turning to human breast tissue samples, they found that more aggressive tumors have higher levels of the enzyme that converts cholesterol into 27-HC. In breast cancer patients with estrogen receptor-positive tumors, the 27 Hydroxycholesterol content in their breast tissue is increased overall, and especially within the tumor itself—so much so that circulating oxysterol levels in the blood may one day be used as a prognostic factor. And “breast cancer patients with low tumor levels of [the enzyme] that breaks down 27-HC did not live as long” as women who can detoxify it better. “The bottom line…is that some estrogen-driven breast tumors may rely on 27-HC to grow when estrogen isn’t available.” And that may explain a second breast cancer mystery.

Over 80 percent of breast cancers start out responding to estrogen, and so what we do is use hormone blockers—either aromatase inhibitors to stop the formation of estrogen in the first place, or tamoxifen to block its action. Despite the efficacy of these drugs, many patients relapse with resistant tumors. And that’s where oxidized cholesterol can come in. 27-HC can fuel breast cancer growth without estrogen, which could explain why sometimes these estrogen blockers don’t work.

And finally, 27-HC may explain why breast cancer patients with higher vitamin D levels appear to live longer. Vitamin D supplementation decreases 27-HC levels in the blood. The best way, though, may be to just lower overall cholesterol. Lower cholesterol, and you lower oxidized cholesterol. So, discovering this role of cholesterol is actually really good news, since “cholesterol is a highly amenable risk factor, either by lifestyle, dietary, or pharmacologic interventions.” The implications of these findings, according to the principal investigator, is that “lowering cholesterol with dietary changes or [drugs] could reduce a women’s breast cancer risk or slow tumor growth.”

Please consider volunteering to help out on the site.

Image credit: Ed Uthman via flickr. Image has been modified.

Motion graphics by Avocado Video

Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

In 1908, the presence of cholesterol crystals was noted “in the proliferating areas of cancers,” suggesting that perhaps cholesterol, in some way, was “associated with the regulation of [cancer] proliferation.” A century later, we now recognize “the accumulation of cholesterol [as] a general feature of cancer tissue, and recent evidence suggests that cholesterol [may indeed play] critical roles in the progression of cancers, including breast, prostate, and colorectal cancers.”

Perhaps that could explain why “egg consumption was associated with increased breast cancer risk.” And, indeed, a systematic review of the evidence suggests that “dietary cholesterol intake increases risk of breast cancer,” and the more cholesterol you eat, the higher the risk appears to go. But, why?

One thought is that the “[p]rolonged ingestion of a cholesterol-enriched diet induces chronic, auto-inflammatory responses,” and we know that “chronic…inflammation can lead to the initiation, promotion, and progression of tumor development.” It’s true that sprinkling some cholesterol on white blood cells in a test tube can trigger the release of inflammatory compounds, and LDL cholesterol can induce breast cancer proliferation and invasion. But again, that’s in vitro, where you can show that like breast cancer cells can migrate nearly twice as far within a day in a petri dish in the presence of LDL cholesterol. But what about in people?

Well, the level of LDL cholesterol in the blood of women diagnosed with breast cancer does appear to be “a predictive factor of breast tumor progression.” About two years after surgery/chemo/radiation, not one of the women in the lowest third of LDL cholesterol levels had a cancer recurrence. The same could not be said for women with higher cholesterol. We know cholesterol can cause inflammation in our artery walls; maybe it’s also playing an effect on breast cancer initiation and progression? They speculate that the high cholesterol levels may have a “cancer-fueling effect.” And indeed, women with breast cancer who happen to be taking cholesterol-lowering statin drugs appear to live about 40 percent longer before the cancer comes back. But the data isn’t good enough to ensure the drug benefits outweigh the risks, though lowering cholesterol with diet, one may be able to get the best of both worlds. But what does this have to do with dietary cholesterol?

Sure, animal studies show that if you feed mice cholesterol, you can accelerate their cancers, “but extrapolation to humans is difficult as dietary cholesterol has limited effects on blood cholesterol levels in humans.” Thus, “dietary cholesterol might [just] be indicative of a lifestyle prone to health-related problems, including cancer.” Maybe people are just more likely to chase bacon and eggs down with a cigarette, compared to oatmeal? It’s hard to imagine how dietary cholesterol alone could promote cancer development. But that all changed recently, with the discovery that 27-Hydroxycholesterol, a metabolite of cholesterol, “can function as an estrogen and increase the proliferation” of most breast cancer cells.

Ah, so it’s not the cholesterol itself, but what it turns into in the body.Scientists have long struggled to understand why women with heart disease risk factors are more likely to develop breast cancer.” Now, perhaps we know. “The discovery that the most abundant oxidized cholesterol metabolite” in our bloodstream can have estrogenic effects may explain the link between high cholesterol and the development and progression of breast cancer and prostate cancer. Yes, 27-Hydroxycholesterol also stimulates the proliferation of prostate cancer cells, boosting growth by about 50 percent.

I’ve explored before the role oxycholesterols may play in mediating pro-oxidative and pro-inflammatory processes in degenerative diseases, such as Alzheimer’s and heart disease, but now it looks like oxidized cholesterol can play a role in all three stages of tumor development as well: initiation, promotion, and then the progression of cancer. Not just promoting the growth of breast cancer cells, but also inducing their invasion and migration—potentially facilitating breast cancer metastasis through suppressing anti-cancer immunity, and then inducing angiogenesis, helping breast tumors hook up their blood supply.

This is all supported by “several lines of evidence [that point to] a pathologic role” for this cholesterol metabolite. Yeah, you can feed mice cholesterol; their oxysterol levels go up and their tumors accelerate. It “also appears to dramatically hasten the spread, or metastasis, of breast tumors to other organs.” But turning to human breast tissue samples, they found that more aggressive tumors have higher levels of the enzyme that converts cholesterol into 27-HC. In breast cancer patients with estrogen receptor-positive tumors, the 27 Hydroxycholesterol content in their breast tissue is increased overall, and especially within the tumor itself—so much so that circulating oxysterol levels in the blood may one day be used as a prognostic factor. And “breast cancer patients with low tumor levels of [the enzyme] that breaks down 27-HC did not live as long” as women who can detoxify it better. “The bottom line…is that some estrogen-driven breast tumors may rely on 27-HC to grow when estrogen isn’t available.” And that may explain a second breast cancer mystery.

Over 80 percent of breast cancers start out responding to estrogen, and so what we do is use hormone blockers—either aromatase inhibitors to stop the formation of estrogen in the first place, or tamoxifen to block its action. Despite the efficacy of these drugs, many patients relapse with resistant tumors. And that’s where oxidized cholesterol can come in. 27-HC can fuel breast cancer growth without estrogen, which could explain why sometimes these estrogen blockers don’t work.

And finally, 27-HC may explain why breast cancer patients with higher vitamin D levels appear to live longer. Vitamin D supplementation decreases 27-HC levels in the blood. The best way, though, may be to just lower overall cholesterol. Lower cholesterol, and you lower oxidized cholesterol. So, discovering this role of cholesterol is actually really good news, since “cholesterol is a highly amenable risk factor, either by lifestyle, dietary, or pharmacologic interventions.” The implications of these findings, according to the principal investigator, is that “lowering cholesterol with dietary changes or [drugs] could reduce a women’s breast cancer risk or slow tumor growth.”

Please consider volunteering to help out on the site.

Image credit: Ed Uthman via flickr. Image has been modified.

Motion graphics by Avocado Video

Doctor's Note

The video I mentioned is How to Reduce Cholesterol Oxidation. For the role in Alzheimer’s disease, see Oxidized Cholesterol as a Cause of Alzheimer’s Disease.

This is the third in a three-part video series on cholesterol and cancer. In case you missed the first two: Eggs & Breast Cancer and Dietary Cholesterol & Cancer.

There are all sorts of foods that can decrease breast cancer risk, though, and even improve survival. See, for example:

Best way to get D? See The Best Way to Get Vitamin D: Sun, Supplements, or Salons? and The Risks & Benefits of Sensible Sun Exposure.

If you haven’t yet, you can subscribe to my videos for free by clicking here.

92 responses to “Oxidized Cholesterol 27HC May Explain 3 Breast Cancer Mysteries

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      1. Yes, clap, clap, clap, clap for simple solutions.

        I am going to be giving my brother Brazil nuts tomorrow.

        The fine print in the other video said that kidney cancer was correlated with cholesterol, too.

        His tumor is wrapped around a blood vessel but hasn’t taken it yet.

        If I can get him to eat low cholesterol and eat 4 Brazil nuts and not have that tumor get the blood vessel, I will be so happy.

  1. “lowering cholesterol with dietary changes or [drugs] could reduce a women’s breast cancer risk or slow tumor growth.” We’ve heard this sort of thing from so many sources about so many things that it is sometime hard to even notice. But given the packed in explanation of progression of processes presented here, this becomes extraordinarily convincing. This looks like material for the presentation of a full semester course complete with most of the research material necessary to develop the conclusions. Understanding the processes by which dietary sources impact our lives is critical to me. I generally don’t trust the assertion until I understand why. And,,, that is why nutritionfacts is so extraordinarily important.

    Oh, and while breast cancer is somewhat less relevant to me than others, knowing that process of initiation and development is certainly pertinent to most other cancers. So now I have a whole new set of materials I must study.

  2. What with the theories that colesteol increase is a sign/symptom of inflammation, protective rather than damaging. All crap? Smart people I know claim this …!

    1. Inflammation is practically the body’s response to everything when it is overfed. This is why most people who are overweight have multiple inflammatory disorders and why ‘the anti-inflammatory diet’ has become popular. I have never heard a smart person claim ‘cholesterol’ is beneficial without identifying the different types of cholesterol. HDL (high density lipoprotein) is thought to be more beneficial whereas LDL (low density lipoprotein) is the bad stuff that a bad diet raises in the human bloodstream.

    2. keto and Atkins diets etc are high in saturated fat. This causes high cholesterol in most people. If yo are selling/promoting such diets, you therefore have to tell your target market that this is actually a good thing – hence the fighting inflammation story (no actual evidence just a story).

      In actual fact cholesterol appears to cause inflammation rather than fight it eg

      ‘Hypercholesterolaemia leads to cholesterol accumulation in macrophages and other immune cells, which promotes inflammatory responses, including augmentation of Toll-like receptor (TLR) signalling, inflammasome activation, and the production of monocytes and neutrophils in the bone marrow and spleen. On a cellular level, activation of TLR signalling leads to decreased cholesterol efflux, which results in further cholesterol accumulation and the amplification of inflammatory responses.’
      https://www.nature.com/articles/nri3793

      ‘Excessive amounts of cholesterol, an abundant and fundamental lipid molecule in mammalian cells, can trigger the development and progression of atherosclerosis. Accumulation of cholesterol in early atherosclerotic lesions results in the formation of macrophage foam cells, and crystalline cholesterol is found as a hallmark of advanced atherosclerotic plaques. Cholesterol crystals can activate a multimolecular signaling complex of the innate immune system, the NLRP3 inflammasome, resulting in a caspase-1 mediated activation and secretion of proinflammatory interleukin-1 family cytokines. Furthermore, crystalline cholesterol is thought to induce plaque rupture by physical disruption of the fibrous cap covering atherosclerotic lesions. Here we review the role of cholesterol deposition and crystallization for inflammatory responses in cardiovascular diseases.’
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623938/

      But why spoil a beautiful story with ugly facts like these? Especially if all you want is an excuse to eat beef and butter? Or sell keto books and diet plans?

      1. Mr. Fumblefingers, interesting connection of excess cholesterol levels and macrophage accumulation. It’s long been known that some macrophages, TAMs (tumor-associated macrophages) not only help tumor cells grow and metastasize, but ” they can also help tumors survive attacks from the immune system, and from currently available treatments.” (https://www.the-scientist.com/features/macrophages-play-a-double-role-in-cancer-29875) Yet TAMs may also “cancer-killing potential…[and] may aid cancer immunotherapies.” (ditto)

        It’s a complicated world. I like making it simpler by eating a plant based whole foods diet. But I wonder why neither I (breast cancer diagnosis 4 years ago) nor my husband (prostate cancer diagnosis 14 years ago) have never heard one peep from any of our doctors about the role of diet on cancer progression/survival? That is the only problem with nutrtionfacts.org: it makes me so angry with the medical profession!! Furious, actually. Probably “excess bile and spleen” stimulated by thoughts of this issue are not conducive to good health…sigh…

        1. Dr. J,
          Am I to understand that you got breast cancer despite eating WFPB and assuming your cholesterol levels were in check?
          If so, what further direction is there for us to take??

          1. Lida, Well I have learned that with my family history, I had a 1 in 2 chance of developing breast cancer. And at the time, I was an ovo-lacto vegetarian, meaning that I ate eggs and dairy products (though for sustainability reasons, not health reasons. As I’ve mentioned previously, I worried that not eating meat was not healthy.) Though I was the oldest in my family at diagnosis, and at the time, I wondered if my vegetarian diet had anything to do with that fact, but concluded that, nah, it didn’t, how could it? I only discovered Nutrition Facts a few years ago when researching nutrition and cancer. My husband and I have since transitioned to plant based whole foods eating after our cancer diagnoses.

            But please understand that reducing the risk of disease occurrence does not mean that the risk goes to zero. There are no guarantees in this life, and we have very little control over what happens. We can only do our best.

            btw, my mother lived to 93 after 3 cancer diagnoses; my maternal aunt died of breast cancer at age 38. Life certainly seems like a crap shoot.

            1. Dr. J,
              Thank you so much for sharing your story. I also experienced breast cancer and tamoxifen. Since I am also experiencing a slew of other health issues, I am trying to follow the WFPB approach in hopes that it may not be too late to reverse or at least ameliorate these conditions. Like the old joke that had I known I would live this long I would have taken better care of myself! I am finding progress to be SLOW however and wonder how long will it take before I actually feel better as a result of these dietary changes and when testing will show that there have been improvements. You are right that life does seem like a crap shoot and I have struggled with trying to understand why some people get a pass while others have more than their fair share of struggles. Trying to adopt this mantra: I can’t go on; I must go on; I will go on.
              Again, thanks for reaching out.

          2. Lida, I think Dr. J. once said she started the WFPB diet sometime after the diagnosis.

            I’m wondering if she said no to the chemo/radiation, and is relying solely on her current diet to cure it. Or if, like a friend of mind, opted for a lumpectomy and five years (count ’em five!) years of daily meds. My friend just started with the meds, and I hope she won’t have horrible side effects from them.

            I avoid all drug –aside from a very rare half-baby aspirin if I have a headache or something. When I was a kid I used to hallucinate if they gave me Robitussin cough syrup. Horrible stuff! As are all drugs, IMO.

            https://www.livestrong.com/article/26217-side-effects-robitussin-cough-syrup/

            1. YR (Mostly WFPB), I followed the recommended treatment plan: surgery, radiation, tamoxifen (instead of aromatase inhibitors). I didn’t discover this website until a year or two after treatment. In fact, I was told to “eat more protein” during radiation — with NO discussion of what I was already eating, and what I should eat more of. So, I increased my egg consumption from 2 to 3 a week. LOL, right? Because eggs are such a perfect source of protein, right?

              I have read that tamoxifen tends to lower cholesterol levels, and that it may lower levels of oxidized cholesterol as well, whereas aromatase inhibitors increase the levels of oxidized cholesterol.

              And I agree with you about drugs: I don’t like to take any. I research the benefits vs the risks, and make decisions based on the information I can find. In some cases, the benefits are not worth the risks — such as chemotherapy, which a study completed a few years after my diagnosis confirmed. There is no perfect answer. We do the best we can.

              1. Dr. J.

                Yes, we do the best we can.

                Cancer being an industry makes it so much more challenging even to get the proper information.

                My brother right now isn’t being given dietary advice for his cancer or his kidneys. I know, from my cousin, that eggs will be what they push on him eventually. Hoping to fill his brain with so many healthy comfort foods that he doesn’t turn that direction.

                I don’t understand that they aren’t saying WFPB or Keto or Vegan Keto or even some of the other diets. Pritikin, DASH, CHIP, Mediterranean. They won’t mention water fasting or mimicking fasting or calorie restriction or Gerson or any of it at all.

                He isn’t being offered immunotherapy and wasn’t even told of the study which is happening at the hospital he is using.

                If you aren’t already up and running it is so hard to catch up and learn everything between diagnoses and treatment.

                I am interacting with a stranger, through a friend, and he listened and started water fasting after one tiny correspondence. I can’t even handle that I couldn’t get my brother to water fast for 48 hours or to take the soups I bought and do Mimicking fasting.

                I am grateful that he is eating the food. That makes me happy.

            2. Hi, YR….I too try to avoid drugs and have resisted efforts by doctors to persuade me to take them. I do, however, take a beta blocker out of necessity and a baby aspirin following a TIA. Hopefully I can get to the summit where the BP meds will not longer be required.

        2. Dr. J.

          I have been reading about that the macrophages double role in cancer and I love when things I am trying to learn come up.

          Hooray, I am learning things.

        3. “it makes me so angry with the medical profession!!”

          Screw them. Stay out of their allopathic clutches altogether and stay or get healthy with a WFPD.

        4. Dr J

          I think the evidence of diet on tumour progression is limited, which is why doctors tend not to mention it. The evidence isn’t strong enough, is largely associational and therefore possibly confounded by other factors like weight loss which may accompany adoption of eg plant based diets. Doctors tend to confine their recommendations to those for which good evidence from interventional studies exists. This is what the American Cancer Society has to say

          ‘Most research on possible links between diet and the risk of breast cancer coming back has looked at broad dietary patterns, rather than specific foods. In general, it’s not clear if eating any specific type of diet can help lower your risk of breast cancer coming back. Studies have found that breast cancer survivors who eat diets high in vegetables, fruits, whole grains, chicken, and fish tend to live longer than those who eat diets that have more refined sugars, fats, red meats (such as beef, pork, and lamb), and processed meats (such as bacon, sausage, luncheon meats, and hot dogs). But it’s not clear if this is due to effects on breast cancer or possibly to other health benefits of eating a healthy diet.

          Two large studies (known as WINS and WHEL) have looked at the effects of lowering fat intake after being diagnosed with early stage breast cancer. One study found that women on a low-fat diet had a small reduction in the risk of cancer coming back, but these women had also lost weight as a result of their diet, which might have affected the results. The other study did not find a link between a diet low in fat and the risk of cancer coming back.

          Many women have questions about whether soy products are safe to eat after a diagnosis of breast cancer. Soy foods are rich sources of compounds called isoflavones that can have estrogen-like properties in the body. However, some recent large studies have not found that soy food intake affects breast cancer coming back or survival rates. While eating soy foods doesn’t seem to pose a risk, the evidence regarding the effects of taking soy or isoflavone supplements is not as clear.

          While the links between specific types of diets and breast cancer coming back are not certain, there are clearly health benefits to eating well. For example, diets that are rich in plant sources are often an important part of getting to and staying at a healthy weight. Eating a healthy diet can also help lower your risk for some other health problems, such as heart disease and diabetes.’
          https://www.cancer.org/cancer/breast-cancer/living-as-a-breast-cancer-survivor/can-i-lower-my-risk-of-breast-cancer-progressing-or-coming-back.html

          1. Mr Fumblefingers, Your quote includes the statement: “But it’s not clear if this is due to effects on breast cancer or possibly to other health benefits of eating a healthy diet.” Does it really matter which it is? If an improvement in breast cancer outcomes is a primary or secondary outcome of a healthy diet?

            I don’t pay any attention to the ACS for several reasons. They include but are not limited to: The low ratings it receives as a charity. The fact that it has a vested interest in treating cancer but not preventing it. Its role in stampeding women into screening programs for breast cancer through FEAR — and before there was evidence about whether such screening programs are effective in preventing deaths from breast cancer (they aren’t — but they sure are effective at generating lots of new patients!!). Its questionable funding and partnerships; “The chief medical officer [Otis W. Brawley, M.D] at the American Cancer Society (ACS) has stepped down reportedly in a disagreement regarding commercial partnerships.” (http://www.thenonprofittimes.com/people/top-doc-at-acs-steps-down/) I actually admire and respect Dr. Brawley.

            Even your quote above provides no evidence or links to any; conclusory statements with no basis provided, thus, no way to evaluate them.

            So, I will provide my doctors with the transcript of the video above with its list of sources (how many references did it cite? 20+? I’ve looked at several of the abstracts, and found other supporting references on my own), and ask them: Why don’t you discuss evidence based nutrition with your patients?

      2. “cholesterol appears to cause inflammation rather than fight it” I do not believe either is true. Rather, hyperlipidemia can be the response, but not in all cases, to chronic or systemic inflammation.

    3. Emma,

      Theories change when science figures out mysteries.

      Don’t look down on them or exalt them. Don’t permanently tie them to any theory.

      I watched a video with Dr. McDougall and he said that he had been evaluating B-12 for 40 years and still reserved the right to change his mind.

        1. Deb, you mentioned looking for vegan pizza recipe. Sue Resig has one, look it up on Utube.
          She has quite a few interesting recipes available.

          1. Wow, Thanks Marilyn!

            I certainly will look it up!

            My cousin brought over a dish for tomorrow. Enchiladas got moved to Friday.

            Pizza is going to be coming soon.

      1. Jon Griffin and others be careful re Dr. G being “not anti statins.

        He is notably concerned on an earlier video at https://nutritionfacts.org/video/statin-muscle-toxicity/.

        The video description: “Video updated 3/5/2012 to reflect new FDA warning labels citing risks of confusion, memory loss, new onset diabetes, and muscle injury. Even people who don’t experience pain or weakness on cholesterol-lowering statin drugs may be suffering muscle damage.”

        The transcript states “Clear evidence of skeletal muscle damage in statin-treated patients—all statin-treated patients.” It finishes as “So we don’t want to be taking this drug unless we really need it. The problem is, because heart disease remains our #1 killer, most everyone does need to take a statin drug like Lipitor every day for the rest of our lives—except for one group. This is from the editor-in-chief of the American Journal of Cardiology: “Only pure vegetarians for practical purposes do not need statins. Most of the rest of us do!” So, it’s our choice.”

        Dr. G’s clear position is that WFPD is best.

        Also note a comment by Dr.Jon, (Health Support Volunteer) of today at 1:53 pm. As a prescribing physician his experiences are cogent and sobering.

  3. Very provocative, interesting video, excellent production values. Thanks! I just finished a low fat breakfast and also took my daily 20 mg of a statin (not kidding).

    In the many snips from publications that zipped by at 78 mph, I’m pretty sure I recall seeing one study (might have been a meta-analysis) where the “significant” 95 % CI on the relative risk of some horrible outcome showed the range [1.01 – 1.08 ]. That’s pretty skinny evidence for any dramatic claim from the study, don’t you think?

  4. Hello Lida, and thank you for your question,

    I am a family physician with a private practice in lifestyle medicine/plant-based nutrition, and am also a volunteer for this website. I don’t know for sure how Dr. G would respond to your question, but I can surmise that his views are similar to mine, based on having watched hundreds of his videos.

    My approach to using pharmaceuticals to lower cholesterol is that I first try very hard to get patients to use all available lifestyle modifications to bring down their cholesterol. That means no animal foods at all, as a starter. But you also need to look at plant-based sources of fat, and especially saturated fat, which is known to raise cholesterol levels. For example, coconut oil (>90%), palm-kernel (>85%), and palm (50%) oils have a higher percent of saturated fat than do pork lard or chicken fat. Even flax-seed oil, which is my own favorite type of oil due to a very favorable (low) omega 6 to omega 3 ratio, contains about 10% saturated fat. Plant-based doctors like Dr. Caldwell Esselstyn, who treat lots of patients with advanced coronary artery disease, are often extremely strict about consuming NO oil of any kind, and even limit nut consumption.

    And of course, it also matters what you DO eat, not just what you don’t eat. Dr. G has done videos on the cholesterol-lowering properties of various foods:
    – Amla berries: https://nutritionfacts.org/video/the-best-food-for-high-cholesterol/
    – Blueberries: https://nutritionfacts.org/video/benefits-of-blueberries-for-heart-disease/
    – Oatmeal and other high-fiber foods: https://nutritionfacts.org/video/can-oatmeal-reverse-heart-disease/

    Besides diet, I recommend my patients to get regular exercise — [see this video by Dr. G: https://nutritionfacts.org/video/halving-heart-attack-risk/%5D;
    and also adequate sleep.

    So, lifestyle intervention can be mild, moderate, or intense, depending on how committed the patient is to lowering cholesterol without drugs.

    Cholesterol-lowering drugs DO work to lower cholesterol, and there are lots of published studies about the benefits of statin drugs in lowering risk of heart attacks. However, the benefits of statin drugs have been over-stated, as Dr. G points out in this video:
    https://nutritionfacts.org/2016/11/08/how-well-do-cholesterol-lowering-drugs-actually-work/

    We doctors have to be practical, though, and try to help the patient in front of us as best we can. So, I DO have patients in my practice who take statin drugs. My goal is to get them off these medications as soon as possible. But if they are not willing to try to get to an optimal lifestyle, they might need to stay on their statin drug, especially if they have known coronary artery disease.

    One last point about statin drugs (and about ANY pharmaceutical). THEY HAVE SIDE EFFECTS — which can be very serious. I had a patient who got peripheral neuropathy from atorvastatin (Lipitor), which caused him to lose all sensation below his knees, and lose a substantial amount of muscle function in his lower legs as well. His cardiologist kept him on the medication for MONTHS after he began complaining of the side effects, until he came back in to see me.

    So, in summary, the issue of “if diet fails” is not straight-forward or “one size fits all”. My guess is that Dr. Greger, like all doctors, cannot afford to be an absolutist, and that he would feel fine about certain patients being on statin drugs, especially if that is an intermediate step on the way to getting the patient to adopt a more healthy lifestyle. I have patients who still eat meat, who still eat dairy, who still don’t get enough exercise or sleep, who have to compromise with a family member who eats a different diet, and all sorts of other problems. But I work with them to improve, as fast as they’re able.

    I hope this helps.
    Dr.Jon
    https://physicianassistedwellness.com
    Health Support Volunteer for NutritionFacts.org

    1. Dr Jon, unfortunately for many of us, a perfect wfpb diet and lifestyle does not lead to instant nirvana. High cholesterol levels persist, even with small doses of statins added, especially in post menopausal women. Fear mongering does not help lower levels. I wish Dr Greger would address this situation. I read other plant-base forums and have found that so many are very disappointed with their results.

      1. Barb, one of my patients, post-menopausal, comes from a family with very high cholesterol, especially high ldl.
        Her doctor had prescribed statins, but she felt awful on them, said the drug caused muscle aches and memory problems.
        She says she is healthy vegan, works out, and her other numbers do reflect that.
        I finally asked her to do a trial of Berberine with Milk Thistle for 3 months. Her total and ldl dropped about 25%, Hdl did go up, triglycerides dropped a bit more. She finally got into normal range, and since she has no heart disease she feels that is ok for her.
        Berberine will also lower HgA1C, but, in her case, hers was a bit high. I wouldn’t worry about dropping HgA1C unless it went below 4.6.

        1. Thank you Marilyn! I will indeed look into it. My A1C is at 4.6 currently. I have put together a Nutrition Facts kind of portfolio diet, and maybe the Berberine would be a positive addition. Another one is 1 tbsp psyllium husk (divided during the day, with water) for every 40 mg lower LDL. And grapefruit also, for a 8 to 10% reduction. (I wonder if there is a vit c connection here?) Thanks again Marilyn, very much appreciated.

        2. Marilyn, Could you please be more specific wrt “Berberine with Milk Thistle”. I assume this was a tea preparation but would like to know the details. Thx.

          1. gengo, I recommended she take 500mg. of Berberine, and 150 mg. of Milk Thistle before meals. i.e. 3x a day.
            Interestingly, this combo in the studies is equivalent to Metformin. The Milk Thistle makes the Berberine more effective.
            Then if cholesterol (or blood sugar really high), Berberine root extract and quercetin before bed.
            The only brands Consumers liked was Thorne and Natural Factors.
            For the root extract I use the Solaray which is 250mg. of Berberine, and 285mg. of Oregon Grape.
            Quercetin dose 500mg. I recommend Jarrow for the Milk Thistle and Quercetin, but other reputable brands would work.
            I do not like grocery store brands.

            Goes without saying I wouldn’t recommend taking both Berberine and Metformin.
            This does not work for everyone, but some people do respond well. And I only do this after I’m sure they have fixed their diet.
            It seems that the people who tend to have problems with statins are athletes and women. Women have more side effects, and they don’t seem to benefit as much. Statins may inhibit muscle healing enough that some athletes notice.

            But women with heart disease benefit from statins. And sometimes just adding Ubiquinol and vitamin K2 takes care of their side effects. So a woman with heart disease should first see if that helps.

            Also, anyone with heart disease should have a ferritin level done. Excess iron is corrosive, and some genetic groups have a high rate of hemochromatosis. I’m always astounded that most cardiologists don’t do this test.

    2. Dr. Jon,

      Thank you for the clinical experience information.

      I love that you added in the Amla and blueberries and oatmeal.

      4 Brazil nuts per month.

      Trying to remember the list

      Soy

      B-vitamins

      D3

      Drinking enough water

    3. Matters have been made much worse with the new AHA guidelines. At 72, no matter what values I put into the new calculator for TC, LDL, HDL etc., it is recommended I be on a statin. I am on a 100% WFP diet with a TC of 137, LDL of 83, exercise every day, low BMI, normal BP, etc, and still my GP says she recommends a low dose statin No mention of possible side effects (my brother had muscle problems from a statin, which fortunately went away after he stopped it and instead opted for a WFP diet, which dropped his LDL below 80). Reading what literature is available to me, there seems to be no sound reason for this recommendation, at least for otherwise low risk people like me.

      1. Gengo

        They usually articulate the reasons why, clearly and in detail in the actual guidelines

        In your case, it is probably because you are between 40 and 75 of age and have an LDL cholesterol score greater than 70 plus some other risk factors You’d have to plough through the guidelines in detail to find the actual studies and trials which support this recommendation.

        https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2018/11/09/14/28/2018-guideline-on-management-of-blood-cholesterol

        1. Tom, Your comment is well taken. My main concern is really that doctors will often not pay attention to the nuances of the guidelines. The statistical models, developed based on populations, are “best educated guesses”, and it is not clear in all cases how to apply them to individuals, especially those like me have no obvious other risk factors like obesity, high blood pressure, diabetes, etc. and who eat a 100% WFP diet and exercise several hours every day.

          Interestingly, I noticed today that the newest calculator https://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/ only provides estimates for 40-59 year olds, which suggests that the ACC lacks confidence in the applicability of the calculator estimates for older people.

          .

          1. I thought that that one was the old ACC calculator? In any event though, if you look at the very bottom of the page, it states that you have to complete certain data fields before you can get an age 40 to age 79 risk estimate.

            Of course, if you don’t like the US calculators, you could always use the UK or European risk calculators instead. They employ slightly different factors/weightings. Perhaps they will give you a different recommendation.

            1. Good suggestion. I’ll try the others out of curiosity but I’m not about to take statins in my situation since I don’t think the evidence of benefit is string enough.

    4. Dr. Jon, thank you for sharing your prospective on statins. I wish all doctors were so caring and would be willing to try lifestyle changes first,

    5. Dr. Jon,
      I am so appreciative of this reply to my question. I find it extremely helpful that it comes from a medical point of view. I am trying hard to avoid having to take statins and trying, instead, to lower my cholesterol and LDL (HDL is very good) through dietary means. I am going to print out your response and savor it and re-read it whenever I have doubts that I have lost my way. Thank you so very, very much!

    6. Dr. Jon,
      I am so appreciative of this reply to my question. I find it extremely helpful that it comes from a medical point of view. I am trying hard to avoid having to take statins and trying, instead, to lower my cholesterol and LDL (HDL is very good) through dietary means. I am going to print out your response and savor it and re-read it whenever I have doubts that I have lost my way. Thank you so very, very much!

    1. Yes, cholesterol can become oxidized. Here is a discussion of this process taken from Dr. Gregers video: https://nutritionfacts.org/video/does-cholesterol-size-matter/
      “We’ve known for decades that LDL cholesterol is bad, but oxidized LDL is even worse. So, her logic goes, since eggs have trace amounts of these antioxidants, the implication is that eggs prevent cholesterol oxidation. But the science shows the exact opposite. Consumption of eggs increases the susceptibility of LDL cholesterol to oxidation. They found that not only does eating eggs raise LDL levels, but also increases LDL oxidizability,”

  5. Any cholesterol consumed in diet is already partially oxidized.The only exception would be breast milk fed directly from the breast to the child.

    Cholesterol exposed to heat, light and/or oxygen begins to oxidize, so foods such as cheese, powered milk, or dehydrated or powered eggs would be prime sources. Cooked or dried meats would also be a prime source. Parmesan cheese sitting on a table for days would probably top the list in this regard.

    Packaged pancake mixes where you just have to add water would be loaded with oxidized cholesterol.

    1. Thanks for posting that YR.. very interesting. I wandered about the NYT many yoga pages/guides just now. They have done a nice job. https://www.nytimes.com/guides/well/yoga-stress At the bottom of that page there is a brief paragraph on how yoga can impact your genes and lower inflammatory response.

      I enjoy 3 hrs of yoga class, 2 spin classes, 2 hrs swimming and endless walking per week. I understand why Dr Ornish has his patients participate in meditation, yoga, or tai chi etc. It’s the one class I don’t want to miss.

      1. Barb, yesterday the Dr. Ornish (written with his wife Anne) was waiting for me at the library. It’s a mighty big bruiser, around 450 pages, including recipes, and I of course had to tote it back home. No big deal, the library is within easy walking distance.

        Good to hear you keep active! I have to, myself, or I go stir crazy — like I’ll probably be this weekend; we’re expecting a lot of snow.

        Anyway, the info re Anne (a pretty gal, BTW; the book shows their pics): “Anne Ornish is vice president of program development at the nonprofit Preventive Medicine Research Institute. She is the creator of the Ornish Lifestyle Medicine digital platform, including Ornish.com and Empower, a turn-key learning management system that trains healthcare professionals and participants throughout the country. Anne Ornish has more than twenty five years of advanced training in yoga and meditation and was featured on the cover of Yoga Journal.”

        Not too shabby! :-)

        1. I ‘spose I should give the title of the book:

          UNDO IT! How Simple Lifestyle Changes Can reverse Most Chronic Diseases, by Dean Ornish, M.D. and Anne Ornish

  6. The nocebo and placebo effects are very powerful but there are limits. Despite decades of frantic positive thinking I am still not filthy rich, incredibly handsome or 21 again. Heck, I wouldn’t mind just one out of the three but no joy. Drat.

    But perhaps it is a good thing to have a fever’d imagination. it certainly sounds preferable to deliberately contracting malaria,dengue or syphilis to fight cancer
    http://www.bbc.com/future/story/20150306-the-mystery-of-vanishing-cancer

    1. Laughing

      I just wrote a text to send to my brother tomorrow telling him to go get all of his vaccinations.

      Wish so much that I could get him to either water fast or mimicking fast.

      Wish I could give him the flu.

      I haven’t even heard of one person having it this year.

      The immune system seems so likely to be the answer to spontaneous remission.

      The fact that they have had some results even with calorie restriction, some people might get diagnosed and not feel hungry for long enough to trigger the immune system response (versus others who would eat more)

      https://www.youtube.com/watch?v=APwnkpD_BfI

      1. “Wish I could give him the flu.”
        – – – – – –

        Deb, that’s a pretty unusual comment, even from you! Were you just testing to see if anybody reads your posts?

        1. YR

          A BBC article linked to in one of my earlier posts discussed spontaneous cancer remissions following a strong immune rection to various infections The others were syphilis, gonorrhea, malaria and dengue etc ……… so the flu definitely seems like the least bad option out of all those for Deb to choose.

  7. Meat is still recommended in the diet, though in small amounts, according to a “comprehensive report that sets out targets on how to feed the world in a way that’s good for human health and the health of the planet…Written by 37 scientists from 16 countries and published Wednesday in the medical journal The Lancet, in conjunction with an advocacy group called the EAT Forum, the report was funded by the Wellcome Trust and Stordalen Foundation…

    People in North America eat more than 6 times the recommended amount of red meat, the report said, while countries in South Asia eat half of what’s recommended…

    The report took pains to say that it wasn’t trying to prescribe to people what to eat or how to eat. It laid out global targets for what constitutes a healthy diet, based on an average intake of 2,500 calories a day. That includes 14 grams, or about half an ounce, of beef or lamb a day. That’s roughly the equivalent of a McDonald’s Quarter Pounder every eight days.

    The report said the largest share of daily calories, 35 percent, should come from whole grains, including rice, wheat and corn, and starchy tubers like potatoes and cassava. The recommendations included unsaturated fats, milk, cheese and nuts, and lots of green vegetables. Overall, the guidelines called for a doubling of global consumption of fruits, nuts, vegetables and legumes, and cutting the consumption of red meat in half…

    The Lancet report also made clear that individual consumer choices would not be enough to avert what the authors called “catastrophic damage to the planet.” ”

    (https://www.nytimes.com/2019/01/16/climate/meat-environment-climate-change.html?action=click&module=Latest&pgtype=Homepage)

    1. An interesting comment from the link you posted, Dr. J.:

      “The meat reduction recommendation received immediate pushback. Even before the release of the Lancet report, the Animal Agriculture Alliance, an industry group, issued a statement extolling the benefits of meat and dairy. It said cutting animal protein could “risk worsening malnutrition, increasing food waste, and distracting from the highest priorities for addressing greenhouse gas emissions.” The group echoed the Lancet report’s recommendation to reduce food waste.”

  8. On the other hand?

    http://www.greenmedinfo.com/blog/underreported-dangers-low-cholesterol

    Cholesterol Is Needed To Fight Cancer: The inverse relationship between cholesterol levels and the risk for a variety of cancers, and mortality associated with cancer, has been known about since the late 80’s.[iii] Since then, the cholesterol-cancer connection has been confirmed over and over again. It is to be expected, therefore, that statin drug use would be linked with increased cancer incidence, which indeed it is.[iv] Even when you take so-called “bad” LDL-cholesterol and administer it to a culture of highly malignant, multi-drug resistant leukemia cells, the cells lose their resistance to chemotherapy. Not exactly what can be characterized as a “bad” substance, now is it? [v]

    1. Bob

      That is just another ‘alternative health’ site fuelled by dangerous ignorance.

      Yes, there is a link between declining cholesterol (that is not the result of healthy lifestyle changes, drugs or surgery) and the risk of having a cancer diagnosis Just as there is a link between unintentional weight loss and the risk of a cancer diagnosis.

      Many cancers are slow growing but all grow by building new cancer cells They do this by robbing the host of energy and nutrients to build the new cells A key component of all cells is cholesterol It is a key construction material used in building new cells and repairing damage caused by injury and disease This is why unintentional cholesterol (and weight) lowering can be a pre-clinical marker of cancer and other diseases There are also studies that suggest that stable low level cholesterol is not associated with increased risk but declining cholesterol is – eg

      ‘Among nearly 6000 healthy Japanese-American men enrolled in the Honolulu Heart Study, they measured total serum cholesterol at two time points, with mortality follow-up extending for up to 16 years. Results showed the expected association of elevated cholesterol with coronary disease. In addition, falling levels of cholesterol were linked to an excess risk of hepatic disease and cancer in particular, whereas low (<4.7 mmol/L, <180 mg/dL) but stable levels over time were not associated with excess risk. Their findings provide evidence that the association previously reported between low cholesterol and noncoronary mortality probably reflected the cholesterol-lowering metabolic consequences of long-term subclinical disease rather than a hazard associated with low cholesterol per se.

      This conclusion is consistent with results of a recent meta-analysis10 of cause-specific mortality (including unpublished data on noncardiovascular causes of death) from 10 large cohort studies and 2 international studies that concluded that reduced serum cholesterol is not related to excess mortality among cohorts of employed individuals, whereas population-based studies did show a relationship. The investigators proposed that the discrepancy in results was probably due to a higher frequency of risk factors associated with low cholesterol, eg, alcohol abuse and ill health, in population-based study samples compared with employed cohorts'

      Two additional pieces of evidence that suggest that low cholesterol is not a causal factor for noncardiovascular disease are the normal to extended life expectancy experienced by individuals with genetically determined hypobetacholesterolemia11 and populations with low average blood cholesterol levels, such as the Japanese and Greeks, who do not exhibit an excess of noncardiovascular disease deaths.12

      One strength of the investigation by Iribarren et al9 is its ability (albeit limited to two measures) to track cholesterol over time. In an effort to eliminate the possible cholesterol-lowering effects of latent disease, previous studies have excluded from analyses deaths within the first 2, 5, or 10 years of follow-up. The results found by Iribarren et al7 suggest that a drop in serum cholesterol may occur over a decade before disease is diagnosed. This is plausible; at least two examples of long-term morbidity leading to cholesterol reduction are hepatitis B virus infection13 and chronic respiratory disease resulting in repeated respiratory infections.14'
      https://www.ahajournals.org/doi/full/10.1161/01.cir.92.9.2365

      In other words low cholesterol may be an effect of cancer not a cause. Indeed if low cholesterol was causal of cancer you would expect that people whose cholesterol was lowered by statins would experience higher rates of cancer They don't. Quite the opposite
      'Based on current evidence from meta-analyses, use of statin decreases the risk of certain cancers, such as colorectal (8%-12%), gastric (27%-44%), hematological (19%), liver (37%-42%), oesophageal (14%-28%), ovarian (21%) and prostate cancer (7%). On the other side, evidence from meta-analyses also suggests that there is no association between statin use and risk of bladder, breast, endometrial, kidney, lung, pancreatic and skin cancers.'
      https://www.wjgnet.com/2308-3840/full/v5/i2/41.html
      In other words lowered cholesterol may be an effect of cancer not a cause. Indeed if low cholesterol was causal of cancer you would expect that people whose cholesterol was lowered by statins would experience higher rates of cancer They don't. Quite the opposite
      'Based on current evidence from meta-analyses, use of statin decreases the risk of certain cancers, such as colorectal (8%-12%), gastric (27%-44%), hematological (19%), liver (37%-42%), oesophageal (14%-28%), ovarian (21%) and prostate cancer (7%). On the other side, evidence from meta-analyses also suggests that there is no association between statin use and risk of bladder, breast, endometrial, kidney, lung, pancreatic and skin cancers.'
      https://www.wjgnet.com/2308-3840/full/v5/i2/41.htm

      Since cancers need to rob their hosts of cholesterol to grow and expand, you would expect that lowering plasma cholesterol would slow the progression of cancer and extend survival. This is what we see happening in eg

      'Use of statins after prostate cancer diagnosis was associated with a decreased risk of prostate cancer death. The risk decrease was dose-dependent and observed especially among patients treated with hormone therapy.'
      https://www.eu-focus.europeanurology.com/article/S2405-4569(16)30052-9/pdf

      'In this large nation-wide cohort of ovarian cancer patients postdiagnostic use of statins was associated with improved survival.'
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5736195/

      Alterantive health sites like Greenmedinfo try to persuade people to avoid potentially lifesaving therapies and may be responsible for many unnecessary early deaths

    2. Dr. J., I’m surprised Fumbles did not pounce on your “Lancet” reference. A while back, I think he called it a “rag,” or something similar. :-)

        1. You mean you never, ever said anything derogatory about The Lancet? For some reason, I thought you had.

          I wish we had a way to check back.

          1. I have no doubt said something less than complimentary about everything and everyone at some stage.. However I am pretty sure that it was a British newspaper probably The Daily Mail that I specifically referred to as a ‘rag’.

            1. Yes, I remember that well….The Daily Mail, for sure. Two or three posters quoted from both papers, and you poo-pooed what they said.

              You probably scared them away….never heard from them again. :-)

              1. As far as the Lancet is concerned, I think I quoted a senior World Health Organization official who criticised a paper on the PURE study as bad science and also criticised The Lancet for publishing it. That doesn’t seem like me making ‘derogatory’ remarks about The Lancet ….. but whatever makes you happy.

                As for scaring people away, perhaps those individuals were just cholesterol and saturated fat trolls who drop in, post the usual pseudoscientific tripe and disappear?

  9. I do not understand why on this site I leave a direct reply to someone’s post but it does not appear where it should. It somehow gets posted elsewhere. This is not good because then the person to whom I am directing a reply may not see it.

  10. Could someone from Dr. Greger’s team respond to this question?

    In the video, Greger quotes this statement from a study: “but extrapolation to humans is difficult as dietary cholesterol has limited effects on blood cholesterol levels in humans.”

    Since you have many videos that show eating cholesterol increases our risk for cardiovascular disease, how am I supposed to understand the above quote?

  11. Hi, Denise B Rose! I think what the researchers mean when they say, “but extrapolation to humans is difficult as dietary cholesterol has limited effects on blood cholesterol levels in humans,” is that there is variability in the degree to which individual humans’ blood cholesterol levels respond to changes in dietary cholesterol. We do not need any dietary cholesterol, because our bodies make all that we need. If we do eat cholesterol, our bodies generally make less, but some people adapt more than others, and if we eat much more than we need, our bodies cannot reduce any further. Saturated fat and trans fat intakes also raise LDL cholesterol levels. The researchers are simply saying that we are not rats or mice, and so results from these animal studies may not directly translate to humans. Dietary cholesterol, trans fats and saturated fats do influence human blood cholesterol levels. It just might not be exactly the same as in laboratory animals. I hope that helps!

    1. NutritionFacts.org | Christine Kestner, MS, CNS, LDN (Health Support Volunteer) commented on Oxidized Cholesterol 27HC May Explain 3 Breast Cancer MysteriesThank you so much Christine for taking the time to write a full response. I have new knowledge as a result. Smiles…

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