Glycemic Index and Glycemic Load
Summary
- The glycemic index (GI) is a measure of the blood glucose-raising potential of the carbohydrate content of a food compared to a reference food (generally pure glucose). Carbohydrate-containing foods can be classified as high- (≥70), moderate- (56-69), or low-GI (≤55) relative to pure glucose (GI=100). (More information)
- Consumption of high-GI foods causes a sharp increase in postprandial blood glucose concentration that declines rapidly, whereas consumption of low-GI foods results in a lower blood glucose concentration that declines gradually. (More information)
- The glycemic load (GL) is obtained by multiplying the quality of carbohydrate in a given food (GI) by the amount of carbohydrate in a serving of that food. (More information)
- Prospective cohort studies found high-GI or -GL diets to be associated with a higher risk of adverse health outcomes, including type 2 diabetes mellitus and cardiovascular disease. (More information)
- Meta-analyses of observational studies have found little-to-no evidence of an association between high dietary GI and GL and risk of cancer. (More information)
- Lowering the GL of the diet may be an effective method to improve glycemic control in individuals with type 2 diabetes mellitus. This approach is not currently included in the overall strategy of diabetes management in the US. (More information)
- Several dietary intervention studies found that low-GI/GL diets were as effective as conventional, low-fat diets in reducing body weight. Both types of diets resulted in beneficial effects on metabolic markers associated with the risk of type 2 diabetes mellitus and cardiovascular disease. (More information)
- Lowering dietary GL can be achieved by increasing the consumption of whole grains, nuts, legumes, fruit, and non-starchy vegetables, and decreasing intakes of moderate- and high-GI foods like potatoes, white rice, white bread, and sugary foods. (More information)
Glycemic Index
Glycemic index of individual foods
In the past, carbohydrates were classified as simple or complex based on the number of simple sugars in the molecule. Carbohydrates composed of one or two simple sugars like fructose or sucrose (table sugar; a disaccharide composed of one molecule of glucose and one molecule of fructose) were labeled simple, while starchy foods were labeled complex because starch is composed of long chains of the simple sugar, glucose. Advice to eat less simple and more complex carbohydrates (i.e., polysaccharides) was based on the assumption that consuming starchy foods would lead to smaller increases in blood glucose than sugary foods (1). This assumption turned out to be too simplistic since the blood glucose (glycemic) response to complex carbohydrates has been found to vary considerably. The concept of glycemic index (GI) has thus been developed in order to rank dietary carbohydrates based on their overall effect on postprandial blood glucose concentration relative to a referent carbohydrate, generally pure glucose (2). The GI is meant to represent the relative quality of a carbohydrate-containing food. Foods containing carbohydrates that are easily digested, absorbed, and metabolized have a high GI (GI≥70 on the glucose scale), while low-GI foods (GI≤55 on the glucose scale) have slowly digestible carbohydrates that elicit a reduced postprandial glucose response. Intermediate-GI foods have a GI between 56 and 69 (3). The GI of selected carbohydrate-containing foods can be found in Table 1.
Measuring the glycemic index of foods
To determine the glycemic index (GI) of a food, healthy volunteers are typically given a test food that provides 50 grams (g) of carbohydrate and a control food (white, wheat bread or pure glucose) that provides the same amount of carbohydrate, on different days (4). Blood samples for the determination of glucose concentrations are taken prior to eating, and at regular intervals for a few hours after eating. The changes in blood glucose concentration over time are plotted as a curve. The GI is calculated as the incremental area under the glucose curve (iAUC) after the test food is eaten, divided by the corresponding iAUC after the control food (pure glucose) is eaten. The value is multiplied by 100 to represent a percentage of the control food (5):
GI = (iAUCtest food/iAUCglucose) x 100
For example, a boiled white potato has an average GI of 82 relative to glucose and 116 relative to white bread, which means that the blood glucose response to the carbohydrate in a baked potato is 82% of the blood glucose response to the same amount of carbohydrate in pure glucose and 116% of the blood glucose response to the same amount of carbohydrate in white bread. In contrast, cooked brown rice has an average GI of 50 relative to glucose and 69 relative to white bread. In the traditional system of classifying carbohydrates, both brown rice and potato would be classified as complex carbohydrates despite the difference in their effects on blood glucose concentrations.
While the GI should preferably be expressed relative to glucose, other reference foods (e.g., white bread) can be used for practical reasons as long as their preparation has been standardized and they have been calibrated against glucose (2). Additional recommendations have been suggested to improve the reliability of GI values for research, public health, and commercial application purposes (2, 6).
Physiological responses to high- versus low-glycemic index foods
By definition, the consumption of high-GI foods results in higher and more rapid increases in blood glucose concentrations than the consumption of low-GI foods. Rapid increases in blood glucose (resulting in hyperglycemia) are potent signals to the β-cells of the pancreas to increase insulin secretion (7). Over the next few hours, the increase in blood insulin concentration (hyperinsulinemia) induced by the consumption of high-GI foods may cause a sharp decrease in the concentration of glucose in blood (resulting in hypoglycemia). In contrast, the consumption of low-GI foods results in lower but more sustained increases in blood glucose and lower insulin demands on pancreatic β-cells (8).
Glycemic index of a mixed meal or diet
Many observational studies have examined the association between GI and risk of chronic disease, relying on published GI values of individual foods and using the following formula to calculate meal (or diet) GI (9):
Meal GI = [(GI x amount of available carbohydrate)Food A + (GI x amount of available carbohydrate)Food B +…]/ total amount of available carbohydrate
Yet, the use of published GI values of individual foods to estimate the average GI value of a meal or diet may be inappropriate because factors such as food variety, ripeness, processing, and cooking are known to modify GI values. In a study by Dodd et al., the estimation of meal GIs using published GI values of individual foods was overestimated by 22 to 50% compared to direct measures of meal GIs (9).
Besides the GI of individual foods, various food factors are known to influence the postprandial glucose and insulin responses to a carbohydrate-containing mixed diet. A recent cross-over, randomized trial in 14 subjects with type 2 diabetes mellitus examined the acute effects of four types of breakfasts with high- or low-GI and high- or low-fiber content on postprandial glucose concentrations. Plasma glucose was found to be significantly higher following consumption of a high-GI and low-fiber breakfast than following a low-GI and high-fiber breakfast. However, there was no significant difference in postprandial glycemic responses between high-GI and low-GI breakfasts of similar fiber content (10). In this study, meal GI values (derived from published data) failed to correctly predict postprandial glucose response, which appeared to be essentially influenced by the fiber content of meals. Since the amounts and types of carbohydrate, fat, protein, and other dietary factors in a mixed meal modify the glycemic impact of carbohydrate GI values, the GI of a mixed meal calculated using the above-mentioned formula is unlikely to accurately predict the postprandial glucose response to this meal (3). Moreover, the GI is a property of a given food carbohydrate such that it does not take into account individuals' characteristics like ethnicity, metabolic status, or eating habits (e.g., the degree to which we masticate) which might, to a limited extent, also influence the glycemic response to a given carbohydrate-containing meal (11-14).
Using direct measures of meal GIs in future trials — rather than estimates derived from GI tables — would increase the accuracy and predictive value of the GI method (2, 6). In addition, in a recent meta-analysis of 28 studies examining the effect of low- versus high-GI diets on serum lipids, Goff et al. indicated that the mean GI of low-GI diets varied from 21 to 57 across studies, while the mean GI of high-GI diets ranged from 51 to 75 (15). Therefore, a stricter use of GI cutoff values may also be warranted to provide more reliable information about carbohydrate-containing foods.
Glycemic Load
The glycemic index (GI) compares the potential of foods containing the same amount of carbohydrate to raise blood glucose. However, the amount of carbohydrate contained in a food serving also affects blood glucose concentrations and insulin responses. For example, the mean GI of watermelon is 76, which is as high as the GI of a doughnut (see Table 1). Yet, one serving of watermelon provides 11 g of available carbohydrate, while a medium doughnut provides 23 g of available carbohydrate.
The concept of glycemic load (GL) was developed by scientists to simultaneously describe the quality (GI) and quantity of carbohydrate in a food serving, meal, or diet. The GL of a single food is calculated by multiplying the GI by the amount of carbohydrate in grams (g) provided by a food serving and then dividing the total by 100 (4):
GLFood = (GIFood x amount (g) of available carbohydrateFood per serving)/100
For a typical serving of a food, GL would be considered high with GL≥20, intermediate with GL of 11-19, and low with GL≤10. Using the above-mentioned example, despite similar GIs, one serving of watermelon has a GL of 8, while a medium-sized doughnut has a GL of 17. Dietary GL is the sum of the GLs for all foods consumed in the diet.
It should be noted that while healthy food choices generally include low-GI foods, this is not always the case. For example, intermediate-to-high-GI foods like parsnip, watermelon, banana, and pineapple, have low-to-intermediate GLs (see Table 1).
Disease Prevention
Type 2 diabetes mellitus
The consumption of high-GI and -GL diets for several years might result in higher postprandial blood glucose concentration and excessive insulin secretion. This might contribute to the loss of the insulin-secreting function of pancreatic β-cells and lead to irreversible type 2 diabetes mellitus (16).
A US ecologic study of national data from 1909 to 1997 found that the increased consumption of refined carbohydrates in the form of corn syrup, coupled with the declining intake of dietary fiber, has paralleled the increased prevalence of type 2 diabetes (17). In addition, high-GI and -GL diets have been associated with an increased risk of type 2 diabetes in several large prospective cohort studies. A recent updated analysis of three large US cohorts indicated consumption of foods with the highest versus lowest GI was associated with a risk of developing type 2 diabetes that was increased by 44% in the Nurses' Health Study (NHS) I, 20% in the NHS II, and 30% in the Health Professionals Follow-up Study (HPFS). High-GL diets were associated with an increased risk of type 2 diabetes (+18%) only in the NHS I and in the pooled analysis of the three studies (+10%) (18). Additionally, the consumption of high-GI foods that are low in cereal fiber was associated with a 59% increase in diabetes risk compared to low-GI and high-cereal-fiber foods. High-GL and low-cereal-fiber diets were associated with a 47% increase in risk compared to low-GL and high-cereal-fiber diets. Moreover, obese participants who consumed foods with high-GI or -GL values had a risk of developing type 2 diabetes that was more than 10-fold greater than lean subjects consuming low-GI or -GL diets (18).
However, a number of prospective cohort studies have reported a lack of association between GI or GL and type 2 diabetes (19-24). The use of GI food classification tables based predominantly on Australian and American food products might be a source of GI value misassignment and partly explain null associations reported in many prospective studies of European and Asian cohorts.
Nevertheless, conclusions from several recent meta-analyses of prospective studies (including the above-mentioned studies) suggest that low-GI and -GL diets might have a modest but significant effect in the prevention of type 2 diabetes (18, 25, 26). Organizations like Diabetes UK (27) and the European Association for the Study of Diabetes (28) have included the use of diets of low GI/GL and high in dietary fiber and whole grains in their recommendations for diabetes prevention in high-risk individuals. The use of GI and GL is currently not implemented in US dietary guidelines (29).
Cardiovascular disease
Observational studies
Numerous observational studies have examined the relationship between dietary GI/GL and the incidence of cardiovascular events, especially coronary heart disease (CHD) and stroke. A meta-analysis of 14 prospective cohort studies (229,213 participants; mean follow-up of 11.5 years) found a 13% and 23% increased risk of cardiovascular disease (CVD) with high versus low dietary GI and GL, respectively (30). Three independent meta-analyses of prospective studies also reported that higher GI or GL was associated with increased risk of CHD in women but not in men (31-33). A recent analysis of the European Prospective Investigation into Cancer and Nutrition (EPIC) study in 20,275 Greek participants, followed for a median of 10.4 years, showed a significant increase in CHD incidence and mortality with high dietary GL specifically in those with high BMI (≥28 kg/m2) (34). This is in line with earlier findings in the Nurses' Health Study (NHS) showing that a high dietary GL was associated with a doubling of the risk of CHD over 10 years in women with higher (≥23 kg/m2) vs. lower BMI (35). A similar finding was reported in a cohort of middle-aged Dutch women followed for nine years (36).
Additionally, high dietary GL (but not GI) was associated with a 19% increased risk of stroke in pooled analyses of prospective cohort studies (32, 37). A meta-analysis of seven prospective studies (242,132 participants; 3,255 stroke cases) found that dietary GL was associated with an overall 23% increase in risk of stroke and a specific 35% increase in risk of ischemic stroke; GL was not found to be related to hemorrhagic stroke (38).
Overall, observational studies have found that higher glycemic load diets are associated with increased risk of cardiovascular disease, especially in women and in those with higher BMIs.
GI/GL and cardiometabolic markers
The GI/GL of carbohydrate foods may modify cardiometabolic markers associated with CVD risk. A meta-analysis of 27 randomized controlled trials (published between 1991 and 2008) examining the effect of low-GI diets on serum lipid profile reported a significant reduction in total and LDL-cholesterol independent of weight loss (15). Yet, further analysis suggested significant reductions in serum lipids only with the consumption of low-GI diets with high fiber content. In a three-month, randomized controlled study, an increase in the values of flow-mediated dilation (FMD) of the brachial artery, a surrogate marker of vascular health, was observed following the consumption of a low- versus high-GI hypocaloric diet in obese subjects (39).
High dietary GLs have been associated with increased concentrations of markers of systemic inflammation, such as C-reactive protein (CRP), interleukin-6, and tumor necrosis factor-α (TNF-α) (40, 41). In a small 12-week dietary intervention study, the consumption of a Mediterranean-style, low-GL diet (without caloric restriction) significantly reduced waist circumference, insulin resistance, systolic blood pressure, as well as plasma fasting insulin, triglycerides, LDL-cholesterol, and TNF-α in women with metabolic syndrome. A reduction in the expression of the gene coding for 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, in blood cells further confirmed an effect for the low-GI diet on cholesterol homeostasis (42). Well-controlled, long-term intervention studies are needed to confirm the potential cardiometabolic benefits of low GI/GL diets in people at risk for CVD.
Cancer
Evidence that high-GI or -GL diets are related to cancer is inconsistent. A recent meta-analysis of 32 case-control studies and 20 prospective cohort studies found modest and nonsignificant increased risks of hormone-related cancers (breast, prostate, ovarian, and
By Dr. Mercola Statin cholesterol-lowering drugs are widely touted as the best way to lower your cholesterol and thereby prevent a heart attack. They're recommended to people who have "high cholesterol," those who have heart disease, and even for some healthy people as a form of preventive medicine. Statins are among the most widely prescribed drugs on the market, with more than 1 in 4 Americans over 45 taking them. This already inflated number is set to increase significantly due to draft recommendations issued earlier this year by the U.S. Preventive Services Task Force (USPSTF). This federal advisory board recommended statin treatment for people between the ages of 40 and 75 with a 10 percent or greater risk of heart problems in the next 10 years (based on the 2013 AHA-ACC online calculator1) — even if they have not had a previous heart attack or stroke. Needless to say, if you're a U.S. adult aged 40 or beyond, there's a good chance your doctor may bring up statins at your next visit, so you need to do your homework to determine if these drugs are truly right for you — and there's a good chance they're not. 1. They Don't Work Statin drugs work to lower cholesterol, and as your levels fall, you may assume that is proof that you're getting healthier and lowering your risk of heart disease and heart attack. But that would be far from the truth. There is far more that goes into your risk of heart disease than your cholesterol levels. Further, there is evidence showing that statins may actually make your heart health worse and only appear effective due to statistical deception. One report published in the Expert Review of Clinical Pharmacology concluded that statin advocates used a statistical tool called relative risk reduction (RRR) to amplify statins' trivial beneficial effects.2 If you look at absolute risk, statin drugs benefit just 1 percent of the population. This means that out of 100 people treated with the drugs, one person will have one less heart attack. This doesn't sound so impressive, so statin supporters use a different statistic called relative risk. Just by making this statistical sleight of hand, statins suddenly become beneficial for 30 to 50 percent of the population. As STATS at George Mason University explained, "An important feature of relative risk is that it tells you nothing about the actual risk."3 2. Statins Reduce CoQ10 Statins deplete your body of coenzyme Q10 (CoQ10), which accounts for many of their devastating results. Although it was proposed to add a black box warning to statins stating this, the U.S. Food and Drug Administration (FDA) decided against it in 2014. CoQ10 is used for energy production by every cell in your body, and is therefore vital for good health, high energy levels, longevity, and general quality of life. CoQ10's reduced form, ubiquinol, is a critical component of cellular respiration and production of adenosine triphosphate (ATP). ATP is a coenzyme used as an energy carrier in every cell of your body. When you consider that your heart is the most energy-demanding organ in your body, you can surmise how potentially devastating it can be to deplete your body's main source of cellular energy. So while one of statins' claims to fame is warding off heart disease, you're actually increasing your risk when you deplete your body of CoQ10. The depletion of CoQ10 caused by the drug is why statins can increase your risk of acute heart failure. So if you're taking a statin drug, you MUST take Coenzyme Q10 as a supplement. If you're over 40, I would strongly recommend taking ubiquinol instead of CoQ10, as it's far more effectively absorbed by your body. In every study conducted so far, ubiquinol has been shown to be far more bioavailable than the non-reduced form (CoQ10). Dr. Steven Sinatra,cardiologist and founder of the New England Heart Center, recommends taking at least 100 milligrams (mg), but preferably 200 mg of high-quality CoQ10 or ubiquinol daily. One study in the European Journal of Pharmacology showed that ubiquinol effectively rescued cells from the damage caused by the statin drug simvastatin, thereby protecting muscle cells from myopathies.4 The other part most people don't realize is that CoQ10 and ubiquinol are lipid-soluble materials biosynthesized in your blood. The carrier is the blood lipid cholesterol. The ubiquinol actually keeps your LDL (often referred to as the "bad" cholesterol) reduced, as it's an exceptionally potent antioxidant. Reduced LDL cholesterol isn't bad cholesterol at all. Only the oxidized version will cause a problem. So by reducing CoQ10 production in your body, you're also removing the mechanism that keeps your LDL cholesterol from doing harm in your body. 3. Statins Reduce Vitamin K2 A new finding was published in March 2015, and it is not yet widely known. Research published in Expert Review of Clinical Pharmacology revealed that, in contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, the drugs may instead actually stimulate atherosclerosis and heart failure.5 There were several physiological mechanisms discussed in the study that show how statin drugs may make your heart health worse, one being that they inhibit the synthesis of vitamin K2. Vitamin K2 protects your arteries from calcification. Without it, plaque levels worsen. Vitamin K2's biological role is to help move calcium into the proper areas in your body, such as your bones and teeth. It also plays a role in removing calcium from areas where it shouldn't be, such as in your arteries and soft tissues. According to a 2009 Dutch study, vitamin K2 is associated with reduced vascular calcification even at small dietary intakes.6 Statin drugs inhibit the function of vitamin K2 in your body, which means taking them may put you at risk of vitamin K2 deficiency, a condition known to contribute to a number of chronic diseases, including: Osteoporosis Heart disease Heart attack and stroke Inappropriate calcification, from heel spurs to kidney stones Brain disease Cancer 4. Statins Reduce Ketone Production Statins lower cholesterol by inhibiting the enzyme in your liver that produces cholesterol (HMG coenzyme A reductase). Unfortunately this is the same enzyme that produces not only CoQ10 but also ketones, which are crucial nutrients to feed your mitochondria. Ketones are vitally important biological signaling molecules. There are three ketone bodies, acetoacetate, beta hydroxybutyrate, and acetone. They're produced in your liver (they're byproducts of the breakdown of fatty acids) and production increases during fasting.7 As noted in the journal Trends in Endocrinology & Metabolism:8 "Ketone bodies are emerging as crucial regulators of metabolic health and longevity, via their ability to regulate HDAC [histone deacetylases] activity and thereby epigenetic gene regulation." Ketone bodies appear to inhibit HDAC function, which is implicated in the regulation of aging. Further, researchers noted "ketone bodies may link environmental cues such as diet to the regulation of aging."9 5. Increased Risk of Serious Diseases Because statins deplete your body of CoQ10, inhibit synthesis of vitamin K2, and reduce the production of ketone bodies, they increase your risk of other serious diseases. This includes: Cancer Research has shown that long-term statin use (10 years or longer) more than doubles women's risk of two major types of breast cancer: invasive ductal carcinoma and invasive lobular carcinoma.10 According to Dr. Sinatra, statins block the squalene pathway (squalene is the precursor to cholesterol), which he believes is essential in preventing breast cancer. In addition, the use of any statin drug, in any amount, was associated with a significantly increased risk for prostate cancer in a separate study, and there was an increasing risk that came along with an increasing cumulative dose.11 According to a letter to the editor published in the Journal of Clinical Oncology:12 "Several cholesterol-lowering drugs, including statins, have been found to be carcinogenic in rodents in doses that produce blood concentrations of the drugs similar to those attained in treating patients. In accordance, breast cancer occurred in 12 of 286 women in the treatment group of the CARE (Cholesterol and Recurrent Events) trial, but only in one of 290 in the placebo group … In the PROSPER (Prospective Study of Pravastatin in the Elderly at Risk) trial, cancer occurred in 245 of 2,891 patients in the treatment group, but only in 199 of 2,913 in the placebo group … In the SEAS (Simvastatin and Ezetimibe in Aortic Stenosis) trial, cancer occurred in 39 of 944 patients in the treatment group, but only in 23 of 929 in the placebo group … In the two first simvastatin trials, nonmelanoma skin cancer was seen more often as well, and with statistical significance if the results are calculated together … The latter finding may explain the current so-called epidemic of nonmelanoma skin cancer." Diabetes Statins have also been shown to increase your risk of diabetes via a number of different mechanisms. The most important one is that they increase insulin resistance, which can be extremely harmful to your health. Secondly, statins increase your diabetes risk by raising your blood sugar. Statins work by preventing your liver from making cholesterol. As a result, your liver returns the sugar to your bloodstream, which raises your blood sugar levels. These drugs also rob your body of certain valuable nutrients, which can also impact your blood sugar levels. Two nutrients in particular, vitamin D and CoQ10, are both needed to maintain ideal blood glucose levels. A 2011 meta-analysis confirmed the higher the dosage of statin drugs being taken, the greater the diabetes risk. The "number needed to harm" for intensive-dose statin therapy was 498 for new-onset diabetes — that's the number of people who need to take the drug in order for one person to develop diabetes.13 In even simpler terms, 1 out of every 498 people who are on a high-dose statin regimen will develop diabetes. The following scientific reviews also reached the conclusion that statin use is associated with increased incidence of new-onset diabetes: • A 2010 meta-analysis of 13 statin trials, consisting of 91,140 participants, found that statin therapy was associated with a 9 percent increased risk for incident diabetes.14 Here, the number needed to harm was 255 over four years, meaning for every 255 people on the drug, one developed diabetes as a result of the drug in that period of time. • In a 2009 study, statin use was associated with a rise of fasting plasma glucose in patients with and without diabetes, independently of other factors such as age, and use of aspirin, β-blockers, or angiotensin-converting enzyme inhibitors.15 The study included data from more than 345,400 patients over a period of two years. On average, statins increased fasting plasma glucose in non-diabetic statin users by 7 mg/dL, and in diabetics, statins increased glucose levels by 39 mg/dL. Neurodegenerative Diseases Cholesterol is also essential for your brain, which contains about 25 percent of the cholesterol in your body. It is critical for synapse formation, i.e. the connections between your neurons, which allow you to think, learn new things, and form memories. So perhaps it's not surprising that memory loss is widely reported in association with statin use. Further, remember that statins reduce ketone production. Ketone bodies are used as fuel by your brain, and they have also demonstrated the capacity to protect against neuronal disease, seizures, and age-related brain diseases, such as Alzheimer's, Huntington's, and Parkinson's. Researchers from Penn State College of Medicine even found statins were associated with an increased Parkinson's risk.16 High total cholesterol and LDL were also associated with a lower risk of Parkinson's disease. The study concluded, "Statin use may be associated with a higher PD [Parkinson's disease] risk, whereas higher total cholesterol may be associated with lower risk." Musculoskeletal Disorders Statin users are more likely to suffer from musculoskeletal conditions, injuries and pain than non-users.17 Myalgia, muscle weakness, muscle cramps, rhabdomyolysis, autoimmune muscle disease, and tendinous diseases have all been reported in association with statin use. One reason for this may be statins' interference with selenium-containing proteins. Selenoproteins such as glutathione peroxidase are crucial for preventing oxidative damage in your muscle tissue. As reported by Wellness Resources:18 "Blocking the selenoprotein enzyme glutathione peroxidase is akin to pouring gasoline on the fire of inflammation and free radicals, which damages muscle tissue. In fact, the scientists described this blocking of the selenoproteins reminiscent of selenium deficiency induced heart failure, known as Keshan's disease first identified in the 1930s." Further, according to a study published in JAMA Internal Medicine:19 " … [S]tatin use is associated with an increased likelihood of diagnoses of musculoskeletal conditions, arthropathies, and injuries … Several factors may explain the musculoskeletal AEs [adverse events] of statin therapy, including the inhibitory effect on coenzyme Q10 synthesis, selenoprotein synthesis, and the mitochondrial respiratory chain. In addition, in vitro studies indicated that statins may affect apoptosis genes; misregulation of apoptosis is associated with myopathy. Pathologic studies also have shown that statin use may be associated with myopathy in the presence of normal creatine kinase levels, even in the absence of symptoms. Statin-associated necrotizing autoimmune myopathy was noted to persist or progress despite cessation of statin therapy." Cataracts An objective review of PubMed, EMBASE, and Cochrane review databases found that for every 10,000 people taking a statin, there were 307 extra patients with cataracts.20 This was supported by a separate JAMA study, which further revealed that the risk of cataracts is increased among statin users compared with non-users.21 Cataract is a clouding of your eye lens and is a main cause of low vision among the elderly. If you decide to take a statin, a vitamin K2 supplement is highly recommended. MK-7 is the form you'll want to look for in supplements; it's extracted from the Japanese fermented soy product called natto. Professor Cees Vermeer, one of the world's top vitamin K2 researchers, recommends between 45 mcg and 185 mcg daily for adults. You must use caution on the higher doses if you take anticoagulants, but if you are generally healthy and not on these types of medications, I suggest 150 mcg daily. You'll also need to make sure you take CoQ10 or ubiquinol (the reduced form) with it. One study evaluated the benefits of CoQ10 and selenium supplementation for patients with statin-associated myopathy.22 Compared to those given a placebo, the treatment group experienced significantly less pain, decreased muscle weakness and cramps, and less fatigue. Are you looking for a non-drug way to boost your heart health? Here are some of my top recommendations:Friday, September 14, 2018
Statin Side Effects: 5 Reasons Why You Should Not Take Statins
5 Great Reasons Why You Should Not Take Statins
5 Reasons Why You Should Not Take Statins
If You Take Statins, Be Sure You Also Take Vitamin K2 and CoQ10
How to Protect Your Heart Health
Thursday, September 13, 2018
Wednesday, September 12, 2018
Tuesday, September 11, 2018
13+ Useful Glasses Hacks
13+ Useful Glasses Hacks Every Four-Eyes Should Know
Whether you're like me and have to wear glasses 24/7, only need them for reading, or just like to rock a great pair of shades, we all deal with similar issues.
From loose screws to slippery nose grips, glasses can be as annoying as they are useful. But when it's the difference between seeing clearly or not, sometimes we need to get creative.
1. Raid your junk drawer when a screw goes missing.
Most optometrist offices and glasses stores will replace lost screws, sometimes even for free, but that doesn't help when you can't see to drive to the store.
Thankfully, toothpicks, twist ties, safety pins, and other bits or bobs can work as a temporary fix. Just avoid glue.
2. If you notice the screw's loose before it escapes, nail polish will help secure it.
Tighten the screw first, and then apply a coat of clear polish. It doesn't have to be clear, of course, but then it would be pretty obvious that you had nail polish on your glasses.
3. Find your glasses in the dark by adding a little glow.
A stripe of glow-in-the-dark paint or tape will allow you to find it without turning on the lights. You could also use some of those glowing star stickers we all loved as kids.
4. If you don't use a case, your clock can help.
Make a habit of placing your glasses in front of your alarm clock. Even if the light is dim, it will lead your hand in the right direction. If you use your phone as an alarm, set your glasses right on top.
5. Of course, no list of hacks would be complete without the basic do-it-all: tape.
Use it to secure arms or bridges until you can get them fixed, or even use washi tape to change up your look.
In high school, I turned out to be allergic to the metal inside the arms of a pair of my glasses. I rocked tape for a year.
6. Do your glasses keep sliding down your nose? Eye shadow primer can help.
Whether it's sweat or your foundation, a bit of moisture can cause your glasses to slip. Applying a touch of primer to the sides of your nose will add a bit of extra grip.
It's a makeup hack even a lazy girl like me can get behind.
7. Make a magnetic, adjustable shirt clip.
I've broken a few pairs of glasses due to them falling off my shirt collar. This hack by angie_byr on Instructables uses a plastic straw and magnets to solve that problem.
By heating up the straw over a candle, you can make it easier to bend and glue around the arms of your glasses.
Attach magnets to the straw and they'll stick to each other through the fabric of your shirt, keeping them from slipping out. It's pretty genius.
8. Remove scratches with toothpaste.
The micro-abrasives inside toothpaste are perfect for buffing away scratches on your lenses without damaging them. Wipe it over the lenses and rub lightly with a soft cloth before rinsing the paste away.
9. Use a piece of rubber tubing to hold fit-over shades or safety glasses in place.
Fitting a second pair of frames over top of your regular set can be a struggle. There's no one size fits all. Rubber tubing can easily hold that second set in place while you work.
10. DIY Adjustable Lanyard With Paracord
Even if you don't need to wear your glasses all the time, you still need to keep them close. This hack from jdtwelve12 on Instructables makes an easy lanyard for hanging them around your neck.
Old people are notorious for wearing their glasses around their neck, but don't knock it if it works.
This one uses basic paracord and a couple of simple knots to make a fully adjustable lanyard that'll keep your reading glasses where you can find them.
11. Use hot glue as a temporary nose guard.
Can you technically wear glasses with a missing nose guard? Yes, but it hurts! Hot glue can act as a temporary fix. Is there anything hot glue can't do?
12. Lose your glasses? Your phone can help!
Sadly, this only works for nearsighted folks, but it's darn handy! Open your phone's camera and use it to look around. The camera will focus on what's far away while you hold it close enough so you can see the screen.
13. Make your own glass lens cleaner.
It's easy to make your own cleaner at home, so why bother buying it? The most basic recipe involves mixing some rubbing alcohol into warm water with a few drops of dish soap.
14. You can also make a version without alcohol or soap.
If you want to avoid anything processed, try this citrus and vinegar cleanser instead. Soak lemon peels in vinegar for a few weeks and then strain into a container with equal parts water.
15. With online shopping making glasses cheaper, you're going to need a way to store your collection.
This project shared by kokoleo on Instructables is easy and cute. Start with a tall, skinny piece of sturdy fabric and a tie. Yes, a business suit tie.
Sew the tie onto the fabric, creating pockets just large enough to hold a pair of glasses.
Then just attach to a dowel and hang.
This would work great for a sunglasses collection, too.
16. Keep glasses that are slightly too wide from sliding down your nose with hair elastics.
They will add a bit of extra bulk if the arms are too wide. You could use regular elastics, but the fabric-covered hair ties are thicker and softer.
17. If your slipper bridge is the problem, there are even products specifically made to help.
Nerdwax and products like it add a bit of friction to your nose, keeping those frames in place longer.
18. Glasses-wearers all agree that the 3D movie fad was not meant for us.
I definitely want to spend extra on a movie ticket for the privilege of wearing a second pair of glasses over my prescription pair. Arg.
But Sebbel shared a great hack on Instructables.
You just need some thin, sturdy cardboard and a pair of the lenses from your local cinema.
Hey, they give them out for free anyway! Cut out the cardboard using the template Sebbel provides and glue the lenses from the 3D glasses into it.
Now you can fit the lenses over your own glasses, comfortably.
19. Really, Instructables is the place to be if you're looking for great hacks for your glasses.
It makes sense, since so many people wear them in the world. I really like this DIY case shared by jessyratfink.
It's super easy and looks great.
Since my last case has gone MIA (again), I may make this for myself this weekend. Because, really, the best hack for your glasses is to protect them from damage with a good case.
20. At the end of the day, microfiber cloths are always going to be your best friend.
Seriously, keep these things everywhere, and be sure to wash them regularly. You can even cut larger cloths into smaller pieces for all of your on-the-go cleaning needs.
21. There are a few places where wearing your glasses just doesn't make sense — like the shower, for example.
To avoid mixing up your bottles of shampoo and conditioner in there, place a large rubber band around one of them to distinguish it from the other.
22. Foggy glasses are just as annoying and useless as no glasses at all, so to avoid fogging up your lenses, clean them with shaving cream.
Doing so will create a protective film on the glass, which will keep it from fogging.
23. To fix a pair of crooked glasses, place them on a flat surface to gauge the symmetry of each side.
Make all necessary adjustments until both sides of the glasses are resting flat.