Glucosamine
- ccRCC is highly Glycolytic, has minimal mitochondrial capacity and is highly sensitive to Glycolysis inhibitors such as DCA, Fenbenzadole, Quercetin etc. [ref]
- Glucosamine is a mild inhibitor of glycolysis, this creates ROS and cellular stress, upregulating the use of mitochondria.
Significantly inhibited the proliferation of renal cancer 786-O and Caki-1 cells in a dose-dependent manner. Glucosamine up-regulated cell cycle inhibitors p21 and p53.
- After 1500mg glucosamine, serum HS-CRP concentrations were 23% lower compared to placebo (P = 0.048) in a human trial.
Has no effect on fasting blood glucose levels, glucose metabolism, or insulin sensitivity at any oral dose level in healthy subjects, individuals with diabetes, or those with impaired glucose tolerance.
Extended life span of nematodes, ageing mice, mice and worms.
Mimics low carb diet (via glycolisis inhibition), and probably makes it easier to stick to it.
Regular use is associated with reduced all cause mortality (18-39%) in epidemiological studies.
Anti-proliferative potential of Glucosamine in renal cancer cells via inducing cell cycle arrest at G0/G1 phase
Background
Renal cell carcinoma (RCC) is one of the most common types of cancer in urological system worldwide. Recently, the anticancer role of Glucosamine has been studied in many types of cancer. The aim of this study was to investigate the effects of Glucosamine on RCC.
Methods
The effects of Glucosamine on RCC cell proliferation and apoptosis were investigated by MTT assay and Annexin V-FITC Apoptosis assay, respectively in vitro. Cell cycle was detected by flow cytometry after treatment with Glucosamine. Protein levels of several cell cycle associated markers were examined by Western Blot.
Results
Our data showed that Glucosamine significantly inhibited the proliferation of renal cancer 786-O and Caki-1 cells in a dose-dependent manner. Besides, Glucosamine treatment resulted in cell cycle arrest at G0/G1 phase in both cell lines. Meanwhile, the expression of several regulators that contribute to G1/S phased transition, such as Cyclin D1, CDK4 and CDK6, were significantly down-regulated with the up-regulation of cell cycle inhibitors, p21 and p53, after treatment with glucosamine. However, the apoptosis rate of RCC cells was down-regulated when treatment with Glucosamine at 1 mM and 5 mM, while up-regulated at 10 mM.
Conclusions
Our findings indicated that Glucosamine inhibited the proliferation of RCC cells by promoting cell cycle arrest at G0/G1 phase, but not promoting apoptosis. The present results suggested that Glucosamine might be a potential therapeutic agent in RCC treatment in the future.
Randomized trial of glucosamine and chondroitin supplementation on inflammation and oxidative stress biomarkers and plasma proteomics profiles in healthy humans (link)
Methods: We conducted a randomized, double-blind, placebo-controlled, cross-over study to assess the effects of glucosamine hydrochloride (1500 mg/d) plus chondroitin sulfate (1200 mg/d) for 28 days compared to placebo in 18 (9 men, 9 women) healthy, overweight (body mass index 25.0-32.5 kg/m2) adults, aged 20-55 y. We examined 4 serum inflammatory biomarkers: C-reactive protein (CRP), interleukin 6, and soluble tumor necrosis factor receptors I and II; a urinary inflammation biomarker: prostaglandin E2-metabolite; and a urinary oxidative stress biomarker: F2-isoprostane. Plasma proteomics on an antibody array was performed to explore other pathways modulated by glucosamine and chondroitin.
Results: Serum CRP concentrations were 23% lower after glucosamine and chondroitin compared to placebo (P = 0.048). There were no significant differences in other biomarkers. In the proteomics analyses, several pathways were significantly different between the interventions after Bonferroni correction, the most significant being a reduction in the "cytokine activity" pathway (P = 2.6 x 10-16), after glucosamine and chondroitin compared to placebo.
Conclusion: Glucosamine and chondroitin supplementation may lower systemic inflammation and alter other pathways in healthy, overweight individuals. This study adds evidence for potential mechanisms supporting epidemiologic findings that glucosamine and chondroitin are associated with reduced risk of lung and colorectal cancer.
Glucosamine: The new metformin? | Interview with Dr. Michael Ristow (part ii)
You’re a big proponent of a particular intervention that plays off of mitohormesis to increase lifespan–glucosamine. How did this compound come to your attention, and what’s so great about it?
Well, back in 2007 when we showed that increased ROS extends lifespan in C. elegans, we used a compound that completely blocks glucose metabolism, deoxyglucose. Since the cell can’t metabolize glucose anymore, it enters an energy deficit similar to starvation, and responds by switching on its mitochondria. So we tried giving deoxyglucose to mice, but it turned out to be toxic, because having no glucose metabolism is probably not healthy in mammals. Another group at the NIA found the same thing.
Then a student in my lab said, “Why don’t we use glucosamine?” Glucosamine only slightly inhibits glucose metabolism (glycolysis), and it’s known to be completely harmless to humans. It’s like the cell being on a diet: it still activates its mitochondria, still produces a bit more ROS, but not to the excessive level that it would with deoxyglucose. So we fed C. elegans glucosamine, and they lived longer. If we gave them antioxidants in parallel, the effect was gone, which suggested that the benefits were due to increased ROS production. Then we took two year old mice, which is equivalent to something like 55 or 60 in humans, and gave them glucosamine, which caused both males and females to live longer. The effect was stronger in females, but it was independently detectable in both sexes.
While we did that, there was an epidemiological study done in Washington state with data from 88,000 people, and it showed that those people who regularly took glucosamine had about a 20% lower risk of death. And that’s huge, 20% is a lot. Now, this doesn’t establish causality–it’s just an association, and it may be due to other factors. But even after correcting for variables like lifestyle and exercise and so forth, this difference remained.
So it’s already used in humans?
Yes, it has a longstanding track record. Millions of people use it to improve arthritis and cartilage problems. They’re mostly elderly people, because the older you get the more likely you are to have joint problems, and it’s questionable whether it really works for that purpose. There are hundreds of studies out there claiming that glucosamine does or doesn’t improve joint health, and I can’t really say whether it does any good in that regard, but it does have a really outstanding safety record.
With glucosamine there aren’t really any side effects whatsoever, unlike with metformin, which is the subject of a high profile study that’s still in planning at Albert Einstein College of Medicine. Metformin has been off the market for several decades in Europe because of toxicity and so on. So in that regard I think glucosamine has a much better track record.
You mentioned that glucosamine is like putting the cell on a diet. What exactly does that mean?
Glucosamine interferes with one of the enzymes used in glycolysis, or the breakdown of glucose into lactate or pyruvate. So now the mitochondria have to try to burn other sources of energy instead, including fat and some amino acids. What glucosamine essentially does is mimic a low carb diet, because the cell is forced to activate the mitochondria to survive. It has to produce its ATP from mitochondrial metabolism, which will produce free radicals that then act as signals to the rest of the cell.
Since glucose and most sugars can be metabolized without the mitochondria, they won’t cause any free radicals to be produced and mitohormesis won’t be activated. And that’s why carbs, and especially glucose, are so dangerous. If a cell is totally happy not to use its mitochondria, all the inductions of stress defense systems that come with mitohormesis won’t occur anymore.
Does glucosamine do this as well as a ketogenic diet might?
Scientifically I can’t answer that, because it would require a direct comparison, but mechanistically everything points in that direction.
In fact, metformin does something very similar by blocking glucose production in the liver. So the liver produces glucose when there isn’t enough energy available, and metformin interferes with that, which causes a deficit in carbohydrate metabolism.
Speaking of metformin, do you think there will be a TAME trial for glucosamine?
There should be. I think it’s long overdue. It’s an ideal supplement because it’s cheap, there’s no IP attached to it, and it could improve healthspan significantly at almost no cost. A yearly dose is about $15. And the return on investment for both insurers and individuals would be significant.
How does glucosamine stack up against metformin, in terms of evidence of effectiveness?
The evidence for glucosamine in C. elegans and mice is about the same as for metformin. In humans there is evidence that type 2 diabetics live longer if they take metformin than if they don’t, but this doesn’t apply to the general public. Whereas the evidence for glucosamine is in normal, healthy people, which is obviously a different target group.
So type 2 diabetics live longer when they take metformin, but that’s in comparison with having no therapy, or with other diabetic drugs, where patients have improved blood glucose but shorter lives. That’s really a disaster for the pharmaceutical industry, because diabetics would be better off not taking anything than most diabetic drugs, and metformin is the only exception.
I can easily anticipate that metformin will also extend lifespan in healthy people, but that still needs to be proven, because that data isn’t out there yet like it is for glucosamine. And I totally endorse the metformin trial, and I hope they’ll find the funding for that. But I think glucosamine is an equally justifiable candidate, and an even better candidate if you consider the safety record.
d-Glucosamine supplementation extends life span of nematodes and of ageing mice, 2014
d-Glucosamine (GlcN) is a freely available and commonly used dietary supplement potentially promoting cartilage health in humans, which also acts as an inhibitor of glycolysis. Here we show that GlcN, independent of the hexosamine pathway, extends Caenorhabditis elegans life span by impairing glucose metabolism that activates AMP-activated protein kinase (AMPK/AAK-2) and increases mitochondrial biogenesis. Consistent with the concept of mitohormesis, GlcN promotes increased formation of mitochondrial reactive oxygen species (ROS) culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation or impairment of aat-1-expression abolishes GlcN-mediated life span extension in an NRF2/SKN-1-dependent fashion. Unlike other calorie restriction mimetics, such as 2-deoxyglucose, GlcN extends life span of ageing C57BL/6 mice, which show an induction of mitochondrial biogenesis, lowered blood glucose levels, enhanced expression of several murine amino-acid transporters, as well as increased amino-acid catabolism. Taken together, we provide evidence that GlcN extends life span in evolutionary distinct species by mimicking a low-carbohydrate diet.
[10 g / kg in the diet]
Association of habitual glucosamine use with risk of cardiovascular disease: prospective study in UK Biobank (link)
In this large prospective study, habitual glucosamine use was associated with a 15% lower risk of total CVD events and a 9%-22% lower risk of individual cardiovascular events (CVD death, CHD, and stroke). Such associations were independent of traditional risk factors, including sex, age, income, body mass index, physical activity, healthy diet, alcohol intake, smoking status, diabetes, hypertension, high cholesterol, arthritis, drug use, and other supplement use. In addition, we found that the associations between glucosamine use and CVD outcomes were statistically significantly modified by smoking status.
Comparison with other studies
Our findings are in line with several previous studies that show inverse associations of glucosamine use with CVD risk and mortality. In a cross sectional study of 266 844 Australian participants, glucosamine use was found to be inversely associated with risks of heart attack or angina (odds ratio 0.79, 95% confidence interval 0.73 to 0.86) and other heart diseases (0.82, 0.76 to 0.89).3 In the Vitamins and Lifestyle (VITAL) cohort study, glucosamine use was significantly associated with an 18% lower risk of total mortality.634 Similarly in our study, we found that glucosamine use was consistently associated with lower risks of subtypes of CHD, including fatal and non-fatal CHD. Our lack of statistically significant associations between glucosamine use and subtypes of stroke is probably because of small numbers of participants in the subtype groups.
Biological plausibility
Several potential mechanisms could explain the observed protective relation between glucosamine use and CVD diseases. In the National Health and Nutrition Examination Survey (NHANES) study, regular use of glucosamine was associated with a statistically significant reduction in C reactive protein concentrations, which is a marker for systemic inflammation.35 Animal studies also reported that the anti-inflammatory properties of glucosamine might have a preventive role in the pathophysiology of CVD.1718192021 In addition, a previous study found that glucosamine could mimic a low carbohydrate diet by decreasing glycolysis and increasing amino acid catabolism in mice7; therefore, glucosamine has been treated as an energy restriction mimetic agent.36 Low carbohydrate diets have been related to a reduced risk of CVD in epidemiological studies,89 and several recent diet intervention trials report that a low carbohydrate diet has a protective effect against the development of CVD.10111213141516 Other mechanisms might also be involved, and future investigations are needed to explore the functional roles of glucosamine in cardiovascular health.
Glucosamine for longevity
http://www.anti-agingfirewalls.com/2014/06/09/glucosamine-for-longevity/
The 2010 publication Total mortality risk in relation to use of less-common dietary supplements reported: “Background: Dietary supplement use is common in older US adults; however, data on health risks and benefits are lacking for a number of supplements. Objective: We evaluated whether 10-y average intakes of 13 vitamin and mineral supplements and glucosamine, chondroitin, saw palmetto, Ginko biloba, garlic, fish-oil, and fiber supplements were associated with total mortality. Design: We conducted a prospective cohort study of Washington State residents aged 50–76 y during 2000–2002. Participants (n= 77,719) were followed for mortality for an average of 5 y. Results:A total of 3577 deaths occurred during 387,801 person-years of follow-up. None of the vitamin or mineral 10-y average intakes were associated with total mortality. Among the nonvitamin-nonmineral supplements, only glucosamine and chondroitin were associated with total mortality. The hazard ratio (HR) when persons with a high intake of supplements (≥4 d/wk for ≥3 y) were compared with nonusers was 0.83 (95% CI: 0.72, 0.97;Pfor trend = 0.009) for glucosamine and 0.83 (95% CI: 0.69, 1.00;Pfor trend = 0.011) for chondroitin. There was also a suggestion of a decreased risk of total mortality associated with a high intake of fish-oil supplements (HR: 0.83; 95% CI: 0.70, 1.00), but the test for trend was not statistically significant. Conclusions:For most of the supplements we examined, there was no association with total mortality. Use of glucosamine and use of chondroitin were each associated with decreased mortality.”
How to live longer: The natural supplement shown to slash risk of deadly chronic diseases (link)
Glucosamine is better than Rapamycin for autophagy
https://www.longecity.org/forum/topic/104045-glucosamine-is-better-than-rapamycin-for-autophagy/
I recently added Glucosamine to my stack. During my research, I found support for the following:
Extends average lifespan in mice by 6%
Anti-cancer effects in humans
Activates AMPK (like Metformin and Resveratrol)
Inhibits mTOR (like Rapamycin)
Anti-inflammatory
Increases mitochondrial mass
Mimics low-carb diet
Free from serious side-effects
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Glucosamine is a competitve inhibitor of glucose metabolising enzymes - it doesn't disable the enzymes permanently (that would be uncompetitive inhibition). This means, if the substrate (in this case glucose) is much more abundant, it still is going to "win" most of the time for access to the enzyme.
I'll say it before and I'll say it again: IMO glucosamine is a keto mimetic drug: it impedes glycolysis therefore placing more emphasis on mitochondria to stay healthy. It stands to reason this would make it rather difficult for cancer.
I would stay far away from chondroiton.
Glucosamine alone - no problems. Add in chondroiton - colorectal cancer rates rise.
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Are there any diseases in particular that you expect glucosamine to prevent?
I would expect very clear, direct effects on metabolism, so it should improve fatty liver disease, and probably body weight should go down as the most straightforward sign. Because of the switch to mitochondrial-mediated metabolism, I would also expect cancer rates to drop, and it would probably also have a certain effect on dementia prevention, but big questions there still. And the effect on glucose metabolism and diabetes would directly impact cardiovascular problems and stroke. The evidence for that is much better.
But the idea really is to have a compound that’s directed toward a spectrum of age related diseases, not just a specific disease. That’s the idea with both metformin and glucosamine supplementation. So we’d start these compounds in people who are still healthy, probably around 45 or 50, to prevent bad things from happening when you’re 60 or 65.
Association Between Use of Specialty Dietary Supplements and C-Reactive Protein Concentrations (link)
Using survey-weighted multivariate linear regression, significant reductions in hs-CRP concentrations were associated with regular use of glucosamine (17%, 95% confidence interval (CI): 7, 26), chondroitin (22%, 95% CI: 8, 33), and fish oil (16%, 95% CI: 0.3, 29). No associations were observed between hs-CRP concentration and regular use of supplements containing methylsulfonylmethane, garlic, ginkgo biloba, saw palmetto, or pycnogenol. These results suggest that glucosamine and chondroitin supplements are associated with reduced inflammation in humans and provide further evidence to support an inverse association between use of fish oil supplements and inflammation.
Oral Glucosamine Effect on Blood Glucose and Insulin Levels in Patients With Non-Diabetic Osteoarthritis: A Double-Blind, Placebo-Controlled Clinical Trial
Patients and methods
This placebo-controlled, randomized clinical trial included 40 non-diabetic patients with osteoarthritis (15 males, 25 females, mean age 63.8±7.64 years; range 49 to 80 years). Patients were randomly divided into two equal groups and treated with oral glucosamine sulfate 1500 mg a day or placebo for 90 days. Fasting blood sugar, glucose tolerance test with 75 grams glucose and serum insulin levels, and homeostatic model assessment-insulin resistance were evaluated initially and at the end of intervention.
Results
There were no significant differences between the groups in terms of blood sugar, glucose tolerance test, and insulin levels at the beginning and end of the study. In the oral glucosamine group, there were no significant changes in fasting blood sugar (94.1±7.14 mg/dL versus 93.5±9.45 mg/dL, p=0.15), glucose tolerance test (99.3±8.99 mg/dL versus 103.3±10.1 mg/dL, p=0.07), and homeostatic model assessment-insulin resistance (1.57±0.21 versus 1.48±0.21, p=0.13) after treatment. Also, placebo did not significantly affect serum glucose levels and insulin resistance.
Conclusion
Oral glucosamine with routine dosage was safe in our non-diabetic patients with osteoarthritis and had no significant effect on glucose metabolism and insulin resistance.
Glucosamine Supplements May Reduce Risk of Early Death As Much as Exercise (link)
For the study, King and his research partner Jun Xiang analyzed data from 16,686 adults who were at least 40 years old who completed the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010. They then merged the data with 2015 death rates.
After taking into account age, sex, smoking habits, and activity level, the researchers found that taking glucosamine/chondroitin every day for a year or longer was associated with a 39 percent reduction in early death from any cause.
Regular glucosamine/chondroitin users also had a 65 percent reduction in cardiovascular-related deaths, such as stroke and heart disease.
King’s interest in the supplement started with his own use as a cyclist. “I started taking it for arthritis and cycling. I’m part of a local cycling club—the Country Roads Cyclists—and pretty much everyone in the group also takes it,” King said.
“Then I saw two large studies showing that it could help lower the risk of [early] death, especially from cardiovascular disease, and I thought, I’m going to keep taking it,” King said.
The first was a 2012 study published in the European Journal of Epidemiology that analyzed data from 77,510 supplement users between the ages of 50 to 76. They found that compared to people who never took glucosamine (with or without chondroitin), those who took the supplement had a significantly lower risk of death, and current users had a significantly lower risk of death from cancer.
Compared to nonuse, use of glucosamine was associated with a 20% reduction in lung cancer risk (HR 0.80, 95% CI: 0.65–0.99) after multivariable adjustment. High 10-year use of glucosamine was associated with a linear 23% reduction in risk (HR 0.77, 95% CI: 0.56–1.07; P-trend = 0.04).
In an exploratory analysis conducted within the VITamins And Lifestyle (VITAL) study, glucosamine use was associated with a 27% reduced risk of colorectal cancer (CRC) (HR: 0.73; 95% CI: 0.54, 0.98) [4].
The other was a 2019 study in the British Medical Journal that analyzed data from more than 466,000 adults who completed a questionnaire on supplement use. That paper reported that glucosamine use was linked to a significantly lower risk of heart disease, stroke, and other types of cardiovascular disease.
In vivo antiviral activity of D-glucosamine
Intraperitoneal treatments with D-glucosamine, an inhibitor of the glycosylation of the viral envelope, decreased the growth rate of tumors induced in quails or in chicks by Rous sarcoma virus and increased the survival of mice inoculated with human influenza virus.
MAVS O-GlcNAcylation Is Essential for Host Antiviral Immunity against Lethal RNA Viruses (link)
Authors demonstrate D-glucosamine as a potential broad-spectrum antiviral therapeutic.
Highlights
Our study highlights a critical role of O-GlcNAcylation in regulating host antiviral immunity and validates D-glucosamine as a potential therapeutic for virus infections.
D-glucosamine effectively protects mice against a range of lethal RNA viruses, including human influenza virus.
O-GlcNAc transferase (OGT) deficiency impairs host defense against RNA virus. Mitochondrial antiviral-signaling protein (MAVS) is OGlcNAcylated at multiple sites. O-GlcNAcylation of MAVS is critical for the activation of interferon signaling.
Evaluation of Glucosamine in HSV-Keratitis Therapy
Studies with cell monolayers and the use of an animal model for HSV 1 infection demonstrated clearly that glucosamine decreases the multiplication of HSV 1. There is evidence that during the treatment with glucosamine, new glucosamine-tolerant cells are formed in which the virion assembly is affected. However, the viral protein synthesis still occurs so that the immunological anti-HSV 1 reaction is induced. Use of glucosamine in clinical trials shows that glucosamine is a potential antiviral drug.
Oral glucosamine in doses used to treat osteoarthritis worsens insulin resistance (2007)
Background: Glucosamine is used to treat osteoarthritis. In animals, the compound is known to cause insulin resistance, the underlying abnormality in type 2 diabetes mellitus. Insulin resistance in humans taking oral glucosamine in doses used for osteoarthritis has not been studied.
Methods: Volunteer human subjects (n = 38) without known abnormality of glucose homeostasis had fasting serum glucose, insulin, and lipids determined before and after taking 1500 mg glucosamine by mouth every day for 6 weeks. Fasting insulin and glucose were used to calculate homeostasis model assessment (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI). Vascular elasticity was measured by pulse wave analysis. The paired Student's t test was used to compare baseline with posttreatment values. Pearson's correlation was used to determine the relation of baseline HOMA-IR with changes in other variables.
Results: We found a rise in HOMA-IR after 6 weeks of glucosamine (2.8 versus 3.2, P < 0.04). The fall in HOMA-IR among the subjects was statistically related to a higher baseline HOMA-IR by Pearson's correlation(P < 0.01). A rise in serum triglycerides and a rise in LDL cholesterol were statistically related to baseline HOMA-IR. Small artery elasticity fell, and the decrease was higher in those with the highest baseline HOMA-IR.
Conclusions: Notwithstanding its efficacy remaining in question, glucosamine is widely used as treatment for osteoarthritis, which is a condition associated with both obesity and type 2 diabetes mellitus. Our data indicate that persons with underlying poorer insulin sensitivity are at risk for worsening insulin resistance and vascular function with the use of glucosamine in doses used to treat osteoarthritis.
A comprehensive review of oral glucosamine use and effects on glucose metabolism in normal and diabetic individuals (2010)
Based on available evidence, we conclude that GlcN has no effect on fasting blood glucose levels, glucose metabolism, or insulin sensitivity at any oral dose level in healthy subjects, individuals with diabetes, or those with impaired glucose tolerance.
The effect of glucosamine on glucose metabolism in humans: a systematic review of the literature (2011)
Results
Eleven studies were included. Six studies were randomized controlled trials and the remaining five were prospective studies with or without controls. Four of the studies found decreased insulin sensitivity or increased fasting glucose in subjects taking glucosamine. Three of these were clinical studies using oral glucosamine. Studies that included subjects with baseline impaired glucose tolerance or insulin resistance were more likely to detect an effect on glucose metabolism than studies without such subjects.
Conclusion
Clinical studies, including three using oral glucosamine, have provided mixed evidence about the effect of exogenous glucosamine on glucose metabolism in humans. Therefore, more studies are needed, particularly including subjects at high risk for impairments in glucose homeostasis, before a definite conclusion can be made.
Glucosamine/Chondroitin and Mortality in a US NHANES Cohort, 2020
Background: Limited previous studies in the United Kingdom or a single US state have demonstrated an association between intake of glucosamine/chondroitin and mortality. This study sought to investigate the association between regular consumption of glucosamine/chondroitin and overall and cardiovascular (CVD) mortality in a national sample of US adults.
Methods: Combined data from 16,686 participants in National Health and Nutrition Examination Survey 1999 to 2010, merged with the 2015 Public-use Linked Mortality File. Cox proportional hazards models were conducted for both CVD and all-cause mortality.
Results: In the study sample, there were 658 (3.94%) participants who had been taking glucosamine/ chondroitin for a year or longer. During followup (median, 107 months), there were 3366 total deaths (20.17%); 674 (20.02%) were due to CVD. Respondents taking glucosamine/chondroitin were less likely to have CVD mortality (hazard ratio [HR] = 0.51; 95% CI, 0.28-0.92). After controlling for age, use was associated with a 39% reduction in all-cause (HR = 0.61; 95% CI, 0.49–0.77) and 65% reduction (HR = 0.35; 95% CI, 0.20–0.61) in CVD mortality. Multivariable-adjusted HR showed that the association was maintained after adjustment for age, sex, race, education, smoking status, and physical activity (all-cause mortality, HR = 0.73; 95% CI, 0.57–0.93; CVD mortality, HR = 0.42; 95% CI, 0.23–0.75).
Conclusions: Regular intake of glucosamine/chondroitin is associated with lower all-cause and CVD mortality in a national US cohort and the findings are consistent with previous studies in other populations. Prospective studies to confirm the link may be warranted. ( J Am Board Fam Med 2020;33:842–847.)
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