Health Journal Online

Category: Nutrition

  • IBD and Cannabis 

    IBD and Cannabis 

    Smoking cannabis may help with symptoms of inflammatory bowel disease (IBD) in the short term, but it may make the long-term prognosis worse.

    As this study asks, “Medical Marijuana: A Panacea or Scourge?” For 5,000 years, cannabis “has been used throughout the world medically, recreationally, and spiritually.” It was even prescribed by American physicians “for a plethora of indications” from the mid-19th century to the 1930s, a fact that’s often used by medical marijuana proponents as evidence justifying the modern medical applications.” But the field of old-timey medicine is “fraught with potions and herbal remedies,” not to mention bloodletting and other questionable and harmful remedies.

    Skeptics criticize the medical marijuana movement as the “‘medical excuse marijuana’ movement,” insinuating that children with epilepsy and the terminally ill are being “used as a ‘Trojan horse’ for the legalization of recreational cannabis use” or to peddle “outlandish claims” about “miracle cancer cures,” frustrating researchers in the field who just want to get at the science.

    For example, what about the therapeutic use of cannabis for inflammatory bowel diseases like Crohn’s disease and ulcerative colitis? Conventional therapies work mainly by suppressing the immune system to try to tamp down inflammation. “Given the limited therapy options and known adverse side effects with chronic use” from these drugs, people suffering from these diseases often need to have inflamed sections of their bowels removed surgically, so it’s clear why there’s so much interest in alternative approaches.

    About one in six IBD patients who use marijuana say it helps with their symptoms, so researchers decided to put it to the test. Thirteen patients with IBD were given a third of a pound of marijuana to smoke at their leisure over a period of three months, and they reported feeling significantly better with “reported improvement in general health perception, social functioning, ability to work, physical pain, and depression.” There wasn’t a control group, so it’s unknown if they would have improved anyway or what role the placebo effect may have played. It’s like some of the studies of cannabis used for pediatric epilepsy that had response rates exceeding 30 percent and a frequency cut in half in a third of the kids. Amazing results until you realize you can sometimes get similarly amazing responses from giving kids nothing but a sugar pill placebo, as seen below and at 2:21 in my video Friday Favorites: Cannabis for Inflammatory Bowel Disease (IBD). That’s why it’s critical to do randomized, double-blind, placebo-controlled trials, but there weren’t any on cannabis and IBD until 2013. 

    For 21 patients with Crohn’s disease, nothing seemed to help. So researchers randomized them to either smoke two joints a day of marijuana or a look-alike placebo. The results? Ninety percent of those in the cannabis group got better, compared to only 40 percent in the placebo group. Shown below and at 3:11 in my video is a graph of their symptom scores. As you can see, there was no big change in the placebo group over the two-month study, but the cannabis group cut their symptoms by about half. 

    The researchers acknowledge that long-term cannabis use is not without risks, but it may be a cakewalk compared to the potential adverse—and even life-threatening—side effects of some of the more powerful conventional therapies, so the study was heralded in a paper entitled “High Hope for Medical Marijuana in Digestive Disorders.”

    The study was funded by a medical marijuana advocacy organization, the main supplier in the country, in fact. So, expectations may have been placed on the participants about how much better they would feel—in other words, they may have been primed for the placebo effect. But the researchers controlled for that, right? Those getting the real cannabis did significantly better than those randomized to get the placebo. But the point of a placebo is that it is indistinguishable from the real thing, so the participants don’t know which group they’re in—the control group or the treatment group. How can that be accomplished with a psychoactive drug? It can’t, which is the problem. The researchers tried to hide which group participants were in by only recruiting patients who had never tried cannabis before in the hopes that they wouldn’t notice placebo pot, but, unsurprisingly, most of them did. So, we’re basically left with another unblinded study. The researchers asked a bunch of subjective questions, like “How are you feeling?” and those who pretty much knew they were taking the drug said they were feeling better.

    There were no significant changes in objective lab values, like CRP, a sign of inflammation, so perhaps the “cannabis may simply be masking symptoms without affecting intestinal inflammation.” Another indicator that it may not be affecting the course of the disease itself is how quickly the symptoms rebound. Two weeks after the study ended, those in the cannabis group were right back to where they started, as shown here (see week 10) and at 5:05 in my video. 

    So, “there was no difference in objective inflammatory markers to indicate disease modification. Given the rapid rebound…to pretreatment levels after the 2-week washout period, it seems more plausible that cannabis ameliorated the symptoms of Crohn’s disease, rather than actually modulating the disease.” That may be, but the symptoms are terrible. A reduction in pain is a reduction in pain. Indeed, “from the point of view of the patients, a marked symptomatic improvement and ability to resume normal life is not trivial, even if inflammation persists.” Of course, what if cannabis somehow makes the disease worse in the long run?

    A survey study published the following year found that cannabis provided the same immediate symptomatic relief but was associated with a worse disease prognosis over time. Patients with IBD reported that cannabis improved their pain, cramping, and diarrhea, but use for more than six months by Crohn’s patients appeared to be a strong predictor of them ending up in surgery; they had five times the odds of going under the knife. There are two possible explanations for this: It’s quite possible that the increased disease severity led to the cannabis use and not the other way around. The alternative explanation: “Cannabis use may worsen the prognosis of IBD, leading to greater surgeries and hospitalizations.”

    This is why we need prospective clinical trials where people are followed over time to see which came first. Until then, perhaps we should consider cannabis use for IBD as “potentially harmful.” Not just to err on the side of caution, but because there was a study on hepatitis C patients that found that daily cannabis use was associated with nearly seven times the odds of worse liver fibrosis, which is like scar tissue. If cannabis really does make fibrosis worse, that may explain why cannabis users with IBD may be more likely to require surgery. 

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  • Eating to Downregulate a Gene for Metastatic Cancer 

    Eating to Downregulate a Gene for Metastatic Cancer 

    Women with breast cancer should include the “liberal culinary use of cruciferous vegetables.”

    Both the Women’s Intervention Nutrition Study and the Women’s Health Initiative study showed that women randomized to a lower-fat diet enjoyed improved breast cancer survival. However, in the Women’s Healthy Eating and Living Study, women with breast cancer were also randomized to drop their fat intake down to 15 to 20 percent of calories, yet there was no difference in breast cancer relapse or death after seven years.

    Any time there’s an unexpected result, you must question whether the participants actually followed through with study instructions. For instance, if you randomized people to stop smoking and they ended up with the same lung cancer rates as those in the group who weren’t instructed to quit, one likely explanation is that the group told to stop smoking didn’t actually stop. In the Women’s Healthy Eating and Living Study, both the dietary intervention group and the control group started out at about 30 percent of calories from fat. Then, the diet group was told to lower their fat intake to 15 to 20 percent of calories. By the end of the study, they had in fact gone from 28.5 percent fat to 28.9 percent fat, as you can see below and at 1:16 in my video The Food That Can Downregulate a Metastatic Cancer Gene. They didn’t even reduce their fat intake. No wonder they didn’t experience any breast cancer benefit. 

    When you put together all the trials on the effect of lower-fat diets on breast cancer survival, even including that flawed study, you see a reduced risk of breast cancer relapse and a reduced risk of death. In conclusion, going on a low-fat diet after a breast cancer diagnosis “can improve breast cancer survival by reducing the risk of recurrence.” We may now know why: by targeting metastasis-initiating cancer cells through the fat receptor CD36.

    We know that the cancer-spreading receptor is upregulated by saturated fat. Is there anything in our diet that can downregulate it? Broccoli.

    Broccoli appears to decrease CD36 expression by as much as 35 percent (in mice). Of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total risk of cancer and not just getting cancer in the first place, as you can see here and at 2:19 in my video.

    Those with bladder cancer who eat broccoli also appear to live longer than those who don’t, and those with lung cancer who eat more cruciferous veggies appear to survive longer, too.

    For example, as you can see below and at 2:45 in my video, one year out, about 75 percent of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive (the top line in red), whereas, by then, most who had been getting less than half a serving a day had already died from their cancer (the bottom line in green).

    Ovarian cancer, too. Intake of cruciferous vegetables “significantly favored survival,” whereas “a survival disadvantage was shown for meats.” Milk also appeared to double the risk of dying. Below and at 3:21 in my video are the survival graphs. Eight years out, about 40 percent of ovarian cancer patients who averaged meat or milk every day were deceased (the boldest line, on the bottom), compared to only about 20 percent who had meat or milk only a few times a week at most (the faintest line, on the top). 

    Now, it could be that the fat and cholesterol in meat increased circulating estrogen levels, or it could be because of meat’s growth hormones or all its carcinogens. And galactose, the sugar naturally found in milk, may be directly toxic to the ovary. Dairy has all its hormones, too. However, the lowering of risk with broccoli and the increasing of risk with meat and dairy are also consistent with the CD36 mechanism of cancer spread.

    Researchers put it to the test in patients with advanced pancreatic cancer who were given pulverized broccoli sprouts or a placebo. The average death rate was lower in the broccoli sprout group compared to the placebo group. After a month, 18 percent of the placebo group had died, but none in the broccoli group. By three months, another 25 percent of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43 percent of the remaining patients in the placebo group were deceased, along with the first 25 percent of the broccoli group. Unfortunately, even though the capsules for both groups looked the same, “true blinding was not possible,” and the patients knew which group they were in “because the pulverized broccoli sprouts could be easily distinguished from the methylcellulose [placebo] through their characteristic smell and taste.” So, we can’t discount the placebo effect. What’s more, the study participants weren’t properly randomized “because many of the patients refused to participate unless they were placed into the [active] treatment group.” That’s understandable, but it makes for a less rigorous result. A little broccoli can’t hurt, though, and it may help. It’s the lack of downsides of broccoli consumption that leads to “Advising Women Undergoing Treatment for Breast Cancer” to include the “liberal culinary use of cruciferous vegetables,” for example.

    It’s the same for reducing saturated fat. The title of an editorial in a journal of the National Cancer Institute asked: “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” “Although counseling women to consume a healthy diet after breast cancer diagnosis is certainly warranted for general health, the existing data still fall a bit short of proving this will help reduce the risk of breast cancer recurrence and mortality.” But what do we have to lose? After all, it’s still certainly warranted for general health.



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  • Eating to Help Control Cancer Metastasis 

    Eating to Help Control Cancer Metastasis 

    Randomized controlled trials show that lowering saturated fat intake can lead to improved breast cancer survival.

    The leading cause of cancer-related death is metastasis. Cancer kills because cancer spreads. The five-year survival rate for women with localized breast cancer is nearly 99 percent, for example, but that falls to only 27 percent in women with metastasized cancer. Yet, “our ability to effectively treat metastatic disease has not changed significantly in the past few decades…” The desperation is evident when there are such papers as “Targeting Metastasis with Snake Toxins: Molecular Mechanisms.”

    We have built-in defenses, natural killer cells that roam the body, killing off budding tumors. But, as I’ve discussed, there’s a fat receptor called CD36 that appears to be essential for cancer cells to spread, and these cancer cells respond to dietary fat intake, but not all fat.

    CD36 is upregulated by palmitic acid, as much as a 50-fold increase within 12 hours of consumption, as shown below and at 1:13 in my video How to Help Control Cancer Metastasis with Diet.

    Palmitic acid is a saturated fat made from palm oil that can be found in junk food, but it is most concentrated in meat and dairy. This may explain why, when looking at breast cancer mortality and dietary fat, “there was no difference in risk of breast-cancer-specific death…for women in the highest versus the lowest category of total fat intake,” but there’s about a 50 percent greater likelihood of dying of breast cancer with higher intake of saturated fat. Researchers conclude: “These meta-analyses have shown that saturated fat intake negatively impacts breast cancer survival.”

    This may also explain why “intake of high-fat dairy, but not low-fat dairy, was related to a higher risk of mortality after breast cancer diagnosis.” If a protein in dairy, like casein, was the problem, skim milk might be even worse, but that wasn’t the case. It’s the saturated butterfat, perhaps because it triggered that cancer-spreading mechanism induced by CD36. Women who consumed one or more daily servings of high-fat dairy had about a 50 percent higher risk of dying from breast cancer.

    We see the same with dairy and its relationship to prostate cancer survival. Researchers found that “drinking high-fat milk increased the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. Low-fat milk was not associated with such an increase in risk.” So, it seems to be the animal fat, rather than the animal protein, and these findings are consistent with analyses from the Health Professionals Follow-up Study (HPFS) and the Physicians’ Health Study (PHS), conducted by Harvard researchers.

    There is even more evidence that the fat receptor CD36 is involved. The “risk of colorectal cancer for meat consumption” increased from a doubling to an octupling—that is, the odds of getting cancer multiplied eightfold for those who carry a specific type of CD36 gene. So, “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” A cancer diagnosis is often referred to as a ‘teachable moment’ when patients are motivated to make changes to their lifestyle, and so provision of evidence-based guidelines is essential.”

    In a randomized, prospective, multicenter clinical trial, researchers set out “to test the effect of a dietary intervention designed to reduce fat intake in women with resected, early-stage breast cancer,” meaning the women had had their breast cancer surgically removed. As shown below and at 4:02 in my video, the study participants in the dietary intervention group dropped their fat intake from about 30 percent of calories down to 20 percent, reduced their saturated fat intake by about 40 percent, and maintained it for five years. “After approximately 5 years of follow-up, women in the dietary intervention group had a 24% lower risk of relapse”—a 24-percent lower risk of the cancer coming back—“than those in the control group.” 

    That was the WINS study, the Women’s Intervention Nutrition Study. Then there was the Women’s Health Initiative study, where, again, women were randomized to lower their fat intake down to 20 percent of calories, and, again, “those randomized to a low-fat dietary pattern had increased breast cancer overall survival. Meaning: A dietary change may be able to influence breast cancer outcome.” What’s more, not only was their breast cancer survival significantly greater, but the women also experienced a reduction in heart disease and a reduction in diabetes.



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  • Raising the standard in aged care

    Raising the standard in aged care


    In this special episode for National Diabetes Week, we’re joined by dietitian, diabetes educator and self-proclaimed tech nerd, Amy Rush. With over a decade of experience, Amy shares how dietitians can confidently navigate the ever-changing world of diabetes technology to deliver more personalised care.

    Hosted by Brooke Delfino

    Biography

    Amy Rush is an experienced dietitian and diabetes educator with a passion for improving the lives of people living with type 1 diabetes. As Clinical Director of the Type 1 Diabetes Family Centre, she brings over a decade of expertise to her work, combining evidence-based care with a deeply personalised approach. A recognised leader in therapeutic carbohydrate reduction, Amy was a lead author of the 2024 international Therapeutic Carbohydrate Reduction (TCR) guidelines. She’s known for helping people fine-tune the food-insulin relationship using tech like CGMs and pumps, and continues to educate healthcare professionals on practical, person-centred strategies for optimising diabetes care.

     

    In this episode, we discuss:

    • The evolution of diabetes tech (CGMs, insulin pumps and beyond)
    • Using CGM data to tailor nutrition advice
    • Supporting behaviour change and avoiding tech overwhelm
    • Access, equity and future trends in diabetes care

    Additional resources

    The content, products and/or services referred to in this podcast are intended for Health Care Professionals only and are not, and are not intended to be, medical advice, which should be tailored to your individual circumstances. The content is for your information only, and we advise that you exercise your own judgement before deciding to use the information provided. Professional medical advice should be obtained before taking action. The reference to particular products and/or services in this episode does not constitute any form of endorsement. Please see  here  for terms and conditions.


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  • Extreme longevity and health optimization: What it really takes

    Extreme longevity and health optimization: What it really takes

    If so, you don’t have to look very far to find claims about how to improve—no, “optimize”—your health.

    Want to reverse chronic disease? Extend that youthful glow? Live to 115… or forever? Lots of fitness influencers, authors, and podcasters will tell you how to do it.

    In this infographic, we’ll explore.

    By the end of it, you’ll have clarity about how to get the health and longevity you want, while living a life you enjoy.


    You can help people build sustainable nutrition and lifestyle habits that will significantly improve their physical and mental health—while you make a great living doing what you love. We’ll show you how.

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  • Dietary Components That May Cause Cancer to Metastasize 

    Dietary Components That May Cause Cancer to Metastasize 

    Palmitic acid, a saturated fat concentrated in meat and dairy, can boost the metastatic potential of cancer cells through the fat receptor CD36.

    The leading cause of death in cancer patients is metastasis formation. That’s how most people die of cancer—not from the primary tumor, but the cancer spreading through the body. “It is estimated that metastasis is responsible for ~90% of cancer deaths,” and little progress has been made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make matters worse. In an editorial entitled “Therapy-Induced Metastasis,” its authors “provide evidence that all the common therapies, including radiotherapy, chemotherapy, fine needle biopsies, surgical procedures and anaesthesia, have the potential to contribute to tumour progression.” You can imagine how cutting around a tumor and severing blood vessels might lead to the “migration of residual tumour cells,” but why chemotherapy? How might chemo exacerbate metastases? “Despite reducing the size of primary tumors, chemotherapy changes the tumor microenvironment”—its surrounding tissues—“resulting in an increased escape of cancer cells into the blood stream.” Sometimes, chemo, surgery, and radiation are entirely justified, but, again, other times, these treatments can make matters worse. If only we had a way to treat the cause of the cancer’s spreading.

    The development of antimetastatic therapies has been hampered by the fact that the cells that initiate metastasis remain unidentified. Then, a landmark study was published: “Targeting Metastasis-Initiating Cells Through the Fatty Acid Receptor CD36.” Researchers found a subpopulation of human cancer cells “unique in their ability to initiate metastasis”; they all express high levels of a fat receptor known as CD36, dubbed “the fat controller.” It turns out that palmitic acid or a high-fat diet specifically boosts the metastatic potential of these cancer cells. Where is palmitic acid found? Although it was originally discovered in palm oil, palmitic acid is most concentrated in meat and dairy. “Emerging evidence shows that palmitic acid (PA), a common fatty acid in the human diet, serves as a signaling molecule regulating the progression and development of many diseases at the molecular level.” It is the saturated fat that is recognized by CD36 receptors on cancer cells, and we know it is to blame, because if the CD36 receptor is blocked, so are metastases.

    The study was of a human cancer, but it was a human cancer implanted into mice. However, clinically (meaning in cancer patients themselves), the presence of these CD36-studded metastasis-initiating cells does indeed correlate with a poor prognosis. CD36 appears to drive the progression of brain tumors, for example. As seen in the survival curves shown below and at 3:21 in my video What Causes Cancer to Metastasize?, those with tumors with less CD36 expression lived significantly longer. It is the same with breast cancer mortality: “In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels.” That isn’t a surprise, since “CD36 plays a critical role in proliferation, migration and…growth of…breast cancer cells.” If we inhibit CD36, we can inhibit “the migration and invasion of the breast cancer cells.” 

    Below and at 3:46 in my video, you can see breast cancer cell migration and invasion, before and after CD36 inhibition. (The top lines with circles are before CD36 inhibition, and the bottom lines with squares are after.)

    This isn’t only in “human melanoma- and breast cancer–derived tumours” either. Now we suspect that “CD36 expression drives ovarian cancer progression and metastasis,” too, since we can inhibit ovarian cancer cell invasion and migration, as well as block both lymph node and blood-borne metastasis, by blocking CD36. We also see the same kind of effect with prostate cancer; suppress the uptake of fat by prostate cancer cells and suppress the tumor. This was all studied with receptor-blocking drugs and antibodies in a laboratory setting, though. If these “metastasis-initiating cancer cells particularly rely on dietary lipids [fat] to promote metastasis,” the spread of cancer, why not just block the dietary fat in the first place?

    “Lipid metabolism fuels cancer’s spread.” Cancer cells love fat and cholesterol. The reason is that so much energy is stored in fat. “Hence, CD36+ metastatic cells might take advantage of this feature to obtain the high amount of energy that is likely to be required for them to anchor and survive at sites distant from the primary tumour”—to set up shop throughout the body.

    “The time when glucose [sugar] was considered as the major, if not only, fuel to support cancer cell proliferation is over.” There appears to be “a fatter way to metastasize.” No wonder high-fat diets (HFD) may “play a crucial role in increasing the risk of different cancer types, and a number of clinical studies have linked HFD with several advanced cancers.”

    If dietary fat may be “greasing the wheels of the cancer machine,” might there be “specific dietary regimens” we could use to starve cancers of dietary fat? You don’t know until you put it to the test, which we’ll look at next.



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  • Does Black Cumin Seed (Nigella Sativa) Help with Weight Loss? 

    Does Black Cumin Seed (Nigella Sativa) Help with Weight Loss? 

    For three cents a day, black cumin may improve our cholesterol and triglyceride levels, blood pressure, and blood sugar control, as well as accelerate the loss of body fat.

    Black cumin, also known as Nigella sativa or simply “black seed,” is not related to cumin; it’s a member of the buttercup family rather than the carrot family. Black cumin, with its peppery flavor, is a spice commonly used in Indian and Middle Eastern cuisines, but it’s also been prized for its purported medicinal benefits. Described as “a miracle herb,” with mentions going back to the Old Testament, it was found cached in King Tut’s tomb, and it’s been reported that the “Islamic prophet Muhammad once stated that the black seed can heal every disease except death.” Only in the last 50 years or so has it been put to the test, though, culminating in more than a thousand papers published in the medical literature.

    Typical doses used in studies are one or two grams a day, which is only about a quarter teaspoon. This enables researchers to perform randomized, double-blind, placebo-controlled trials by putting the whole-food spice powder into capsules rather than studying a component or extract.

    A systematic review and meta-analysis of randomized, placebo-controlled trials found that daily black cumin consumption significantly improves cholesterol and triglycerides. Researchers also found that it not only improves blood pressure, but it also improves blood sugar control. Some of the results are quite extraordinary. For example, one study found that postmenopausal women randomized to a gram a day (less than a quarter teaspoon) of black cumin powder reduced their LDL cholesterol by 27 percent within two months, significantly better than placebo. Those are the kinds of results we’d expect from a statin drug, yet it was achieved with just a sprinkle’s worth of a simple spice. Black cumin may also help with menopausal symptoms.

    Now, it doesn’t appear to cure anything—a month after stopping the spice, cholesterol levels began to creep back up, for instance, as you can see below and at 2:00 in my video Benefits of Black Cumin Seed (Nigella Sativa) for Weight Loss—but it does appear to be a cheap, safe, effective, and delicious (if you like spice) treatment for some of our deadliest risk factors. And its side effects include loss of appetite and weight loss! 

    The latest systematic review and meta-analysis of randomized controlled weight-loss trials found that about a quarter teaspoon of black cumin powder a day does appear to cause weight loss within a span of a few months. If it really can benefit so many facets of health, why don’t we hear more about it? Why wasn’t I taught about it in medical school? Maybe because there’s little profit motive. Black cumin is just a common, natural spice. The daily dose used in most of these studies would cost about three cents a day. Stockholders won’t be thrilled to sell something that can’t be patented and costs only three pennies a day. Black cumin has become a staple in my family’s daily diet. I keep a pepper mill filled with it right on the kitchen table and grind it onto foods just as I would black pepper—easy and delicious.



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  • Raising the standard in aged care

    Raising the standard in aged care


    With the strengthened Aged Care Quality Standards coming into effect on 1st November 2025, dietitians are more central than ever to aged care quality. In this episode, we’re joined by Louise Murray, APD and Principal Consultant at Nosh Dietitians Co. to unpack what’s changing and how dietitians can step confidently into their evolving roles. Louise explores how we can use our seat at the table to advocate, influence foodservice, and bridge the gap between clinical and catering. From screening to resident feedback loops and 24/7 snack access models, this episode is packed with practical takeaways.

    Hosted by Rebecca Sparrowhawk

    Biography

    Louise Murray is an Accredited Practising Dietitian, specialising in aged care nutrition and food services. She started her career in the hospital setting, but through family connections she started assessing menus in residential aged care 6 months after graduating. This ignited her mission to remove party pies and sausage rolls from aged care menus, and to improve food quality for older people over the past 23 years. Louise’s consultancy Nosh Dietitians specialises in consulting to aged care organisations, seeing clients in the community and mentoring dietitians to become leaders in aged care nutrition.

     

    In this episode, we discuss:

    • What FPIES is and how it differs from other food allergies
    • Recognise the dietitian’s role in diagnosis, nutrition support and care planning
    • Explore approaches to feeding challenges and supporting parent confidence
    • Gain practical guidance for safe and structured food reintroduction

    Additional resources

    • Click here to learn more about Dairy Farmers High Protein milk
    • To connect with your colleagues, join our Australian Aged Care Dietitians LinkedIn Group
    • Connect with Louise Murray on LinkedIn or via her website

     

    The content, products and/or services referred to in this podcast are intended for Health Care Professionals only and are not, and are not intended to be, medical advice, which should be tailored to your individual circumstances. The content is for your information only, and we advise that you exercise your own judgement before deciding to use the information provided. Professional medical advice should be obtained before taking action. The reference to particular products and/or services in this episode does not constitute any form of endorsement. Please see  here  for terms and conditions.


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  • Should We Drink Kombucha 

    Should We Drink Kombucha 

    What are the risks versus benefits of drinking kombucha?

    Is Kombucha Tea Good for You? is one of my first videos. It was featured in a blog entry entitled “NutritionFacts.org: the first month,” where I marveled the video had reached nearly 100,000 people. You can see it below and at 0:20 in my video Kombucha’s Side Effects: Is It Bad for You?. I’m honored to say that we now reach more than 100,000 people a day.

    In that first kombucha video, I profiled a report published in the Journal of Intensive Care Medicine of “a case of kombucha tea toxicity” in which a young man ended up in an acidotic coma. The authors concluded, “While Kombucha tea is considered a healthy elixir, the limited evidence currently available raises considerable concern that it may pose serious health risks. Consumption of this tea should be discouraged, as it may be associated with life-threatening lactic acidosis.” And this was just one of several case reports of “serious, and sometimes fatal, hepatic [liver] dysfunction and lactic acidosis within close proximity of ingestion.”

    For example, there were two cases in Iowa of severe metabolic acidosis, including one death. There was also a triggering of a life-threatening autoimmune muscle disease that required emergency surgery and was “probably related to the consumption of a fermented Kombucha beverage.” Another patient presented with shortness of breath, shaking, and a movement disorder “after consumption of tea and no other medications,” and a middle-aged woman complained of xerostomia, dizziness, nausea, vomiting, headache, and neck pain,” and her symptoms recurred on reingestion of the tea. There was another case of severe metabolic lactic acidosis, as well as a case of hepatotoxicity (liver toxicity) that resolved after stopping kombucha.

    Why these sporadic cases? Maybe some unusual toxins developed in a particular batch. I mean, it is a fermented product, so it’s possible there was just some contamination by a bad bug, like the time people smeared kombucha on their skin because they were told it had “magical healing power.” What it had instead was anthrax. So, even though such reports were rare, I concluded ten years ago that we should probably stick to foods that haven’t put people in a coma. But what about its risks versus benefits? Maybe kombucha is worth it. After all, it’s “reputed to cure cancer,” “eliminate wrinkles,” “and even restore gray hair to its original color”—as “marketed by alternative and naturopathic healers throughout the United States.”

    “Currently, kombucha is alternately praised as ‘the ultimate health drink’ or damned as ‘unsafe medicinal tea.’” It’s been “claimed to be a universal wonderful drug…a potion which improves awareness and concentration, slimming, also purifying, regenerating and life extending.” Which is it? Is it “potion or poison?

    Back in the 1920s, 1930s, and 1940s, there were several medical studies conducted by recognized physicians confirming all sorts of beneficial effects, as you can see below and at 2:55 in my video. 

    I couldn’t wait to read them. Dufrense and Farnworth were cited, and when I went to that paper, I saw the same claim, citing Allen 1998. When I went to that source, I saw the citation is for a random kombucha website, as shown below, and at 3:10 in my video. And guess what? That website’s been defunct since 2001, and “much of the Kombucha information” posted came from comments on some mailing list.

    Finally, in 2003, a systematic review of the clinical evidence that had been published was conducted. “The main result of this systematic review, it seems, is the total lack of efficacy data…No clinical studies were found relating to the efficacy of this remedy.” We just have these cautionary tales, these case reports. So, based on these data, it was concluded that the largely undetermined benefits do not outweigh the documented risks of kombucha. It can therefore not be recommended for therapeutic use.” That was back in 2003, though. How about a 2019 systematic review of the empirical evidence of human health benefit?

    “The nonhuman subjects literature claims numerous health benefits of kombucha,” with “nonhuman” meaning mice and rats. We need human clinical trials, yet there is still not a single controlled human study. (I did find one uncontrolled study purporting to show a significant reduction in fasting and after-meal blood sugars among individuals with type 2 diabetes, though, as seen below and at 4:19 in my video.)

    “Nonetheless,” despite no controlled trials, “significant commercial shelf space is now dedicated to kombucha products, and there is widespread belief that the products promote health.” So, we are left with this extreme disparity between science and belief: “There is no convincingly positive clinical evidence at all; the [health] claims for it are as far-reaching as they are implausible; the potential for harm seems considerable. In such extreme cases, healthcare professionals should discourage consumers from using (and paying for) remedies that only seem to benefit those who sell them.”

    Doctor’s Note:

    Friday Favorites: What Are the Best Beverages? Watch the video to find out. 



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  • Treating Hashimoto’s Disease (Hypothyroidism) Naturally with Diet 

    Treating Hashimoto’s Disease (Hypothyroidism) Naturally with Diet 

    What were the results of a randomized, double-blind, placebo-controlled trial of a daily half teaspoon of powdered black cumin in Hashimoto’s patients?

    “Autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, is an organ-specific autoimmune disorder,” where our body attacks our own thyroid gland, often leading to hypothyroidism due to destruction and scarring of the gland itself. We know there’s a genetic component, since identical twins are more likely to share the disease than fraternal twins. “However, even with identical twins, the concordance rate was only about 50%, emphasizing that important factors such as the environment play a role in disease pathogenesis.” Indeed, even if your identical twin, who has basically your exact same DNA, has the disease, there’s only like a flip of a coin’s chance you’ll get it. Genes load the gun, but the environment may pull the trigger.

    More than 90 synthetic chemicals were noted to show disruption of hormonal balance or thyroid dysfunction.” However, only a few such ‘pollutants show evidence that they contribute to autoimmune thyroid disease.” These include polyaromatic hydrocarbons. Smokers get a lot of them from cigarettes, but in nonsmokers, exposure comes almost entirely from food, as you can see below and at 1:18 in my video Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease. 

    Polycyclic aromatic hydrocarbons are primarily formed when muscle meats, such as beef, pork, fish, or chicken, are cooked using high-temperature methods, such as grilling. PBBs, polybrominated biphenols, are a type of flame-retardant chemical no longer manufactured in the United States, but are still found in the aquatic food chain. PCBs, polychlorinated biphenols, are used in a number of industrial processes and end up in people’s bodies, again, largely through the consumption of fish, but also eggs and other meats, as seen here and at 1:41 in my video.

    So, one might suspect those eating plant-based diets would have lower rates of hypothyroidism, and, indeed, despite their lower iodine intake, vegan diets tended to be protective. But they’ve never been put to the test in an interventional trial. A modification of the Paleolithic diet has been tried in Hashimoto’s patients, but it didn’t appear to improve thyroid function. What did, though, is Nigella Sativa. That name should sound familiar to anyone who’s read my book How Not to Diet or watched my live Evidence-Based Weight Loss presentation. Nigella Sativa is the scientific name for black cumin, which is just a simple spice that’s also used for a variety of medicinal purposes.

    In one study, Hashimoto’s patients received a half teaspoon of powdered black cumin every day for eight weeks in a randomized, double-blind, placebo-controlled trial. Not only was there a significant reduction in body weight, which is why I profiled it in my book, but the black cumin also significantly reduced the thyroid-stimulating hormone, a sign that thyroid function was improving. It even lowered the level of autoimmune anti-thyroid antibodies, as well as increased blood levels of thyroid hormone T3 in these Hashimoto’s patients. In addition, there was a significant drop in Interleukin 23, a proinflammatory cell signal thought to help promote the autoimmune inflammation of the thyroid, which “further confirms the anti-inflammatory nature of the plant.” And what were the side effects? There was a 17 percent drop in “bad” LDL cholesterol, as shown below and at 3:19 in my video.

    Given the fact that patients with Hashimoto’s may be at particularly high risk of developing heart disease, this is exactly the kind of side effects we’d want. “Considering these health-promoting effects of N. Sativa [black cumin], it can be considered as a therapeutic approach in the management of Hashimoto-related metabolic abnormalities.”

    A similar trial failed to find a benefit, though. Same dose, same time frame, but no significant changes in thyroid function. In contrast with the previous study, though, the study participants were not all Hashimoto’s patients, but rather hypothyroid for any reason, and that may have diluted the results. And it’s possible that telling patients to take the black cumin doses with their thyroid hormone replacement therapy may have interfered with its absorption, which is an issue similar to other foods and drugs, and why patients are normally told to take it on an empty stomach. Since there are no downsides—it’s just a simple spice—I figure, why not give it a try? The worst that can happen is you’ll have tastier food.

    Doctor’s Note:

    I get a lot of questions about thyroid function, and I am glad to have been able to do this series. If you missed any of the other videos, see the related posts below.

    For more on black cumin, see my book How Not to Diet and my presentation Evidence-Based Weight Loss. 



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