High-Density Lipoprotein as a Therapeutic Target:A Systematic Review

ontext High-density lipoprotein cholesterol (HDL-C) is a cardiovascular risk factor that is gaining substantial interest as a therapeutic target.

Objectives To review the current and emerging strategies that modify high-density lipoproteins (HDLs).

Data Sources Systematic search of English-language literature (1965-May 2007) in MEDLINE and the Cochrane database, using the key words HDL-C and apolipoprotein A-I and the subheadings reverse cholesterol transport, CVD [cardiovascular disease] prevention and control, drug therapy, and therapy; review of presentations made at major cardiovascular meetings from 2003-2007; and review of ongoing trials from ClinicalTrials.gov and current guidelines from major cardiovascular societies.

Study Selection and Data Extraction Study selection was prioritized to identify randomized controlled trials over meta-analyses over mechanistic studies; identified studies also included proof-of-concept studies and key phase 1 through 3 trials of novel agents. Study eligibility was assessed by 2 authors; disagreements were resolved by consensus with the third.

Data Synthesis Of 754 studies identified, 31 randomized controlled trials met the inclusion criteria. Currently available therapeutic and lifestyle strategies, when optimized, increase HDL-C levels by 20% to 30%. While basic and small pilot studies have shown promise, proof that increasing HDL-C levels confers a reduction in major cardiovascular outcomes independent of changes in levels of low-density lipoprotein cholesterol or triglycerides has been more elusive. Some novel therapeutic agents in human studies appear to effectively increase HDL-C levels, whereas other novel strategies that target HDL metabolism or function may have minimal effect on HDL-C levels.

Conclusions At present there is modest evidence to support aggressively increasing HDL-C levels in addition to what is achieved by lifestyle modification alone. Ongoing clinical trials that target specific pathways in HDL metabolism may help expand cardiovascular treatment options.

Performance Enhancing Drugs: What Parents Need to Know.



In a frequently referenced 1997 Sports Illustrated article, aspiring Olympians were asked two questions; “If you were offered a banned performance-enhancing substance that guaranteed that you would win an Olympic medal and you could not be caught, would you take it?” Remarkably, 195 of 198 athletes said yes. The second question was: “Would you take banned performance-enhancing drugs with a guarantee that you will not be caught, you will win every competition for the next five years, but then will die from adverse effects of the substance?” More than 50 percent of the athletes said yes to this question as well.

Driven by the popularity of sports and athletes’ drive to succeed, the use of ergogenic (performance enhancing) drugs, or PEDs, is at all-time high in the United States today. Fifty-seven percent of high school students play on formal sports teams, and 1-3 million U.S. athletes nationally are taking some form of performance-enhancing drugs. Many of these athletes are youth who use these substances without knowledge of their risks and potential benefits.

Powerful dietary supplements and energy drinks have become part of the PED landscape for some athletes. These drinks and supplements can be found in vitamin and grocery stores and even gas stations. Young people are also using dietary supplements in combination with stimulant prescription medications, such as those used for attention-deficit hyperactivity disorder. Ritalin and other amphetamines are used at surprising rates by teenagers.

In addition to energy and dietary supplements, a growing number of non-elite athletes are using anabolic-androgenic steroids, or AAS, human growth hormones, or HGH, erythropoietin, or EPO and insulin.

A series in Sports Illustrated outlined the breadth of the problem, which encompasses not only players but also media personalities, police and paramilitary personnel and ordinary Americans who want to look, feel and live “at the top of their game.” Eighty percent of PED users are reported to be non-elite athletes.

The most common PEDs are anabolic steroids (eg. testosterone, androstanediol), creatine, stimulants (eg. amphetamine, ephedrine), Erythropoitetin, or EPO, and human growth hormone, or HGH. Although ephedra-based dietary supplements—which have also been used by athletes to reduce fatigue, lose weight and improve mental alertness—were banned by the U.S. Food and Drug Administration in 2004, their place is being taken by an increase in the use of drugs to treat ADHD among athletes.

What’s the appeal?
Athletes may have several reasons for using performance-enhancing drugs. An athlete may want to: build mass and strength of muscles and/or bones; decrease injury recovery time; increase delivery of oxygen to exercising tissues; mask pain; stimulate the body; relax; reduce weight or hide the use of other drugs.

Why are these drugs so appealing to athletes? Besides making muscles bigger, anabolic steroids may help athletes recover from a hard workout more quickly by reducing the muscle damage that occurs during the session. This enables athletes to work out harder and more frequently without overtraining. In addition, some athletes may like the aggressive feelings they get when they take the drugs.

Athletes face enormous pressure to excel in competition. They also know that winning can get them more than a gold medal. A star athlete can earn a lot of money and a lot of fame and athletes only have a short time to do their best work. Athletes know training is the best path to victory, but they also get the message that some drugs and other practices can boost their efforts and give them a shortcut, even as they risk their health and their athletic careers.

Are PEDs ever used for medical reasons? 
Anabolic steroids are used therapeutically in medicine to induce bone growth, stimulate appetite, induce male puberty and treat chronic wasting conditions, such as cancer and HIV/AIDS.

EPO is used in treating anemia resulting from chronic kidney disease and myelodysplasia from the treatment of cancer.

In children, HGH injections are approved for treating short stature of unknown cause as well as poor growth due to a number of medical causes.

In adults, approved uses of HGH include:

  • Short bowel syndrome, a condition in which nutrients are not properly absorbed due to severe intestinal disease or the surgical removal of a large portion of the small intestine
  • HGH deficiency due to rare pituitary tumors or their treatment
  • Muscle-wasting disease associated with HIV/AIDS

What are the consequences of using PEDs improperly? 

Men may develop:

  • Prominent breasts
  • Baldness
  • Shrunken testicles
  • Infertility
  • Impotence

Women may develop:

  • A deeper voice
  • An enlarged clitoris
  • Increased body hair
  • Baldness
  • Infrequent or absent periods

Both men and women might experience:

  • Severe acne
  • Increased risk of tendinitis and tendon rupture
  • Liver abnormalities and tumors
  • Increased low-density lipoprotein, LDL cholesterol (the “bad” cholesterol)
  • Decreased high-density lipoprotein, HDL cholesterol (the “good” cholesterol)
  • High blood pressure/hypertension
  • Heart and circulatory problems
  • Prostate gland enlargement
  • Aggressive behaviors, rage or violence
  • Psychiatric disorders such as depression
  • Drug dependence
  • Infections or diseases such as HIV or hepatitis if you’re injecting the drugs
  • Inhibited growth and development and risk of future health problems in teenagers

What symptoms could help identify someone who is abusing PEDs?

Possible red flags include:

  • Behavioral, emotional or psychological changes — particularly increased aggressiveness (“roid rage”)
  • Changes in body build, including muscle growth, rapid weight gain and development of the upper body
  • Increased acne and facial bloating
  • Needle marks in the buttocks or thighs
  • Enlarged breasts in boys or smaller breasts in girls
  • The bottom line… people who are abusing PEDs will not be themselves.

Is damage done from improper use of PEDs reversible? 

     In males, changes that can be reversed include reduced sperm production and shrinking of the testicles (testicular atrophy). Irreversible changes include male-pattern baldness and breast development (gynecomastia).

In the female body, anabolic steroids cause masculinization. Breast size and body fat decrease, the skin becomes coarse, the clitoris enlarges and the voice deepens. Women may experience excessive growth of body hair but lose scalp hair. With continued administration of steroids, some of these effects become irreversible.

Rising levels of testosterone and other sex hormones normally trigger the growth spurt that occurs during puberty and adolescence and provide the signals to stop growth as well. When a child or adolescent takes anabolic steroids, the resulting, artificially high, sex hormone levels can prematurely signal the bones to stop growing.

Steroid abuse has been associated with cardiovascular diseases, including heart attacks and strokes, even in athletes younger than 30.

Many abusers who inject anabolic steroids may use nonsterile injection techniques or share contaminated needles with other abusers. In addition, some steroid preparations are manufactured illegally under nonsterile conditions. These factors put abusers at risk for acquiring life-threatening viral infections, such as HIV and hepatitis B and C.

The most dangerous of the withdrawal symptoms from anabolic steroid use is depression because it sometimes leads to suicide attempts.


Click to access Honkamp_Youth_Athletes_Feb_08.pdf

Hayashi, A, AAOS Now,” PED use: Legal, natural, and deadly”, Oct 2008
Schafer, M, Porucznik, M, AAOS Now, “If you’re not cheating, you’re not trying”, June 2008

Gastric banding led to improvements in HDL, particle size after 5 years.

Bariatric surgery using gastric banding did not improve LDL cholesterol or LDL particle number or size, despite significant weight loss among patients who underwent the procedure. Results suggest, however, a beneficial HDL remodeling process based on a significant increase in HDL cholesterol and HDL particle size.

Researchers from the New York University Langone Medical Center said the HDL remodeling process persisted up to 5 years after gastric banding.

“Knowing that some studies suggest early improvements in lipids after bariatric surgery, there is a paucity of data regarding changes in the lipoprotein abnormalities characteristic of the dyslipidemia of obesity. What we sought to do was to determine both initial and long-term effects of gastric banding surgery on lipids, with attention to LDL and HDL characteristics,” researcherAmita Singh, MD, from NYU Langone Medical Center in New York, said during a presentation here.

Patients with a BMI of 30 to 40 (n=50) underwent laparoscopic gastric banding. Physical exams and blood samples for nuclear magnetic resonance spectroscopy were performed at baseline and at annual follow-up, which lasted 5 years.

At 1 and 5 years, researchers observed significant increases in HDL cholesterol (P<.001). After 5 years, mean HDL size was significantly increased (9.1 nm at baseline vs. 9.24 nm at 5 years; P<.002), and there was a trend toward increased HDL particle number (33.49 nm/L at baseline vs. 36.75 nm/L; P=.064). Conversely, early reductions in LDL particle number and size were nonsignificant after 5 years.

Metabolic syndrome and percent BMI loss had no effect on changes in particle number or size for both LDL and HDL. However, LDL particle number and LDL cholesterol were significantly correlated at 5 years (P<.001), although HDL cholesterol and HDL particle number were not, the researchers wrote. – by Samantha Costa

  • This study was interesting in the fact that we didn’t see a lot of the changes we expected. Acute weight loss lowers your cholesterol, but losing weight doesn’t lower your cholesterol, and it’s often just dietary changes. It’s interesting to see that, but it’s also limited.
  • Donna M. Polk, MD, MPH
  • Physician at Hartford Hospital (Connecticut)


  • Source: Endocrine Today.


High cardiovascular risk in severely obese young children and adolescents.


Objective To assess the prevalence of cardiovascular risk factors in severely obese children and adolescents.

Methods A nationwide prospective surveillance study was carried out from July 2005 to July 2007 where paediatricians were asked to report all new cases of severe obesity in 2–18-year-old children to the Dutch Paediatric Surveillance Unit. Severe obesity is defined by gender and age-dependent cut-off points for body mass index based on Dutch National Growth Studies corresponding to the adult cut-off point of 35 kg/m2. Paediatricians were asked to complete a questionnaire for every severely obese child regarding socio-demographic characteristics and cardiovascular risk factors (blood pressure, fasting blood glucose and lipids).

Results In 2005, 2006 and 2007, 94%, 87% and 87%, respectively, of paediatricians in the Netherlands responded to the monthly request from the Dutch Paediatric Surveillance Unit and 500 children with newly diagnosed severe obesity were reported. 72.6% (n=363) of paediatricians responded to a subsequent questionnaire. Cardiovascular risk factor data were available in 255/307 (83%) children who were correctly classified as severely obese. 67% had at least one cardiovascular risk factor (56% hypertension, 14% high blood glucose, 0.7% type 2 diabetes and up to 54% low HDL-cholesterol). Remarkably, 62% of severely obese children aged ≤12 years already had one or more cardiovascular risk factors.

Conclusion A high number (2/3) of severely obese children have cardiovascular risk factors. Internationally accepted criteria for defining severe obesity and guidelines for early detection and treatment of severe obesity and comorbidity are urgently needed.

Source: BMJ.



Mood disorder as a specific complication of stroke

Appraising the impact of Folstein et al’s1 1977 report on ‘Mood disorder as a specific complication of stroke’ is a challenging task for someone who did not enter medical school until the mid-1980s. Stroke changed in the 1970s, and the view in retrospect appears unrecognisable. This was a dramatic change, from an intellectual backwater too dull for neurologists to even bother seeing, to become a hot topic: a disease to be studied in mega trials and a standard bearer for evidence based medicine. Prior to the 1970s, with the exception of dysphasia, neuropsychiatric complications had been given scant thought—it was a disorder that affected how people walked. It was recognised that some elderly patients became depressed after stroke but the prevailing view appeared to be “so what, they’re old and infirm, what do you expect?” It is against this backdrop that the work of researchers at John Hopkins has to be judged.

The importance of the paper was perhaps not the findings but the very fact that they published the study at all. Two years earlier their John Hopkins colleague Robert Robinson published a fascinating study demonstrating that experimentally induced strokes in rats led to alteration in cerebral metabolism of catecholamines that correlated with behavioural changes in the rats that mimicked depression.2 Folstein’s data appeared to be an early example of translational research and were widely disseminated as they appeared to link laboratory based neurobiology with clinical practice. Tantalisingly it seemed to offer a human model for studying the anatomy of depression. Appearing, as it did, contemporaneously with the development of cerebral imaging techniques, this was the impetus researchers had needed. Over the next 2 decades, 143 reports were made on this topic. Sadly, the theory of anatomical location of brain lesions as a simplistic explanation for mood disorder did not stand up to scrutiny.3 It was perhaps too good to be true; a salient reminder of the need for confirmation in humans of findings from animal models.

In critical analysis the paper itself has suffered with the passage of time. Epidemiological techniques have advanced, as has expectation of sample sizes and analysis strategies. Future investigators submitting to the journal are unlikely to get a case control study past peer review without any statistical comparisons! But for all that, it is a well written report that gets its key messages across clearly and succinctly, perhaps because the manuscript was not cluttered with t tests and hazard ratios, and that is something editors welcome in any era.

And the key messages were important—the realisation that depression after stroke was not simply an understandable reaction to disability has stood the test of time. We now know that 33% of stroke patients suffer from depression (95% CI 29% to 36%).4 We now know that this depression leads to increased disability5 and probably increased mortality.6 Most importantly, we now know that antidepressants are effective in treating it.7 Countless patients round the world are benefiting from this knowledge and that is an impact that any researcher can be proud of.


  • Competing interests None.
  • Provenance and peer review Commissioned; not externally peer reviewed.


    1. Folstein MF,
    2. Maiberger R,
    3. McHugh PR

. Mood disorder as a specific complication of stroke. J Neurol Neurosurg Psychiatry 1977;40:1018–20.

[Abstract/FREE Full text]

    1. Robinson RG,
    2. Shoemaker WJ,
    3. Schlumpf M,
    4. et al

. Effect of experimental cerebral infarction in rat brain on catecholamines and behaviour. Nature 1975;255:332–4.


    1. Carson AJ,
    2. Machale S,
    3. Allen K,
    4. et al

. Depression after stroke and lesion location: a systematic review. Lancet 2000;356:122–6.

[CrossRef][Medline][Web of Science]

    1. Hackett ML,
    2. Yapa C,
    3. Parag V,
    4. et al

. Frequency of depression after stroke: a systematic review of observational studies. Stroke 2005;36:1330–40.

[Abstract/FREE Full text]

    1. Pohjasvaara T,
    2. Vataja R,
    3. Leppavuori A,
    4. et al

. Depression is an independent predictor of poor long-term functional outcome poststroke. Eur J Neurol 2001;8:315–19.

[CrossRef][Medline][Web of Science]

    1. House A,
    2. Knapp P,
    3. Bamford J,
    4. et al

. Mortality at 12 and 24 months after stroke may be associated with depressive symptoms at 1 month. Stroke 2001;32:696–701.

[Abstract/FREE Full text]

    1. Hackett ML,
    2. Anderson CS,
    3. House A,
    4. et al

. Interventions for treating depression after stroke. Cochrane Database Syst Rev 2008;4:CD003437.

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Top 5 lifestyle changes to reduce cholesterol.

Lifestyle changes can help reduce cholesterol, keep you off cholesterol-lowering medications or enhance the effect of your medications. Here are five lifestyle changes to get you started.

High cholesterol increases your risk of heart disease and heart attacks. You can reduce cholesterol with medications, but if you’d rather make lifestyle changes to reduce cholesterol, you can try these five healthy lifestyle changes. If you’re already taking medications, these changes can also improve their cholesterol-lowering effect.

1. Lose weight

Carrying some extra pounds — even just a few — contributes to high cholesterol. Losing as little as 5 to 10 percent of your body weight can help significantly reduce cholesterol levels.

Start by taking an honest, thorough look at your eating habits and daily routine. Consider your challenges to weight loss and ways to overcome them.

If you eat when you’re bored or frustrated, take a walk instead. If you pick up fast food for lunch every day, pack something healthier from home. If you’re sitting in front of the television, try munching on carrot sticks instead of potato chips as you watch. Take time and enjoy rather than “devouring” your food. Don’t eat mindlessly.

And look for ways to incorporate more activity into your daily routine, such as using the stairs instead of taking the elevator. Take stock of what you currently eat and your physical activity level and slowly work in changes.

2. Eat heart-healthy foods

Even if you have years of unhealthy eating under your belt, making a few changes in your diet can reduce cholesterol and improve your heart health.

  • Choose healthier fats. Saturated fats, found in red meat and dairy products, raise your total cholesterol and low-density lipoprotein (LDL) cholesterol, the “bad” cholesterol. As a general rule, you should get less than 7 percent of your daily calories from saturated fat. Instead, choose leaner cuts of meat, low-fat dairy and monounsaturated fats — found in olive, peanut and canola oils — for a healthier option.
  • Eliminate trans fats. Trans fat can be found in fried foods and many commercial baked products, such as cookies, crackers and snack cakes. But don’t rely on packages that are labeled “trans fat-free.” In the United States, if a food contains less than 0.5 grams of trans fat per serving, it can be labeled “trans fat-free.” Even though those amounts seem small, they can add up quickly if you eat a lot of foods that have a small amount of trans fat in them. Instead, read the ingredients list. You can tell if a food has trans fat in it if it contains partially hydrogenated oil.
  • Limit the cholesterol in your food. Aim for no more than 300 milligrams (mg) of cholesterol a day — less than 200 mg if you have heart disease or diabetes. The most concentrated sources of cholesterol include organ meats, egg yolks and whole milk products. Use lean cuts of meat, egg substitutes and skim milk instead.
  • Select whole grains. Various nutrients found in whole grains promote heart health. Choose whole-grain breads, whole-wheat pasta, whole-wheat flour and brown rice.
  • Stock up on fruits and vegetables. Fruits and vegetables are rich in dietary fiber, which can help lower cholesterol. Snack on seasonal fruits. Experiment with veggie-based casseroles, soups and stir-fries. If you prefer dried fruit to fresh fruit, limit yourself to no more than a handful (about an ounce or two). Dried fruit tends to have more calories than does fresh fruit.
  • Eat foods rich in omega-3 fatty acids. Omega-3 fatty acids can help lower your LDL (“bad”) cholesterol. Some types of fish — such as salmon, mackerel and herring — are rich in omega-3 fatty acids. Other good sources of omega-3 fatty acids include walnuts, almonds and ground flaxseeds.

3. Exercise on most days of the week

Whether you’re overweight or not, exercise can reduce cholesterol. Better yet, moderate physical activity can help raise high-density lipoprotein (HDL) cholesterol, the “good” cholesterol. With your doctor’s OK, work up to at least 30 minutes of exercise a day. Remember that adding physical activity, even in 10-minute intervals several times a day, can help you begin to lose weight. Just be sure that you can keep up the changes you decide to make. Consider:

  • Taking a brisk daily walk during your lunch hour
  • Riding your bike to work
  • Swimming laps
  • Playing a favorite sport

To stay motivated, find an exercise buddy or join an exercise group. And remember, any activity is helpful. Even taking the stairs instead of the elevator or doing a few situps while watching television can make a difference.

4. Quit smoking

If you smoke, stop. Quitting may improve your HDL cholesterol level. And the benefits don’t end there. Just 20 minutes after quitting, your blood pressure decreases. Within 24 hours, your risk of a heart attack decreases. Within one year, your risk of heart disease is half that of a smoker. Within 15 years, your risk of heart disease is similar to someone who never smoked.

5. Drink alcohol only in moderation

Moderate use of alcohol has been linked with higher levels of HDL cholesterol — but the benefits aren’t strong enough to recommend alcohol for anyone who doesn’t already drink. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. Drinking too much alcohol can lead to serious health problems, including high blood pressure, heart failure and stroke.

If lifestyle changes aren’t enough …

Sometimes healthy lifestyle changes aren’t enough to lower cholesterol levels. Make sure the changes you choose to make are ones that you can continue, and don’t be disappointed if you don’t see results immediately. If your doctor recommends medication to help lower your cholesterol, take it as prescribed, but continue your lifestyle changes.

Source: Mayo clinic house call



Organic foods: Are they safer? More nutritious?

Discover the real difference between organic foods and their traditionally grown counterparts when it comes to nutrition, safety and price.

By Mayo Clinic staff

Once found only in health food stores, organic food is now a regular feature at most supermarkets. And that’s created a bit of a dilemma in the produce aisle. On one hand, you have a conventionally grown apple. On the other, you have one that’s organic. Both apples are firm, shiny and red. Both provide vitamins and fiber, and both are free of fat, sodium and cholesterol. Which should you choose?

Conventionally grown produce generally costs less, but is organic food safer or more nutritious? Get the facts before you shop.

Conventional vs. organic farming

The word “organic” refers to the way farmers grow and process agricultural products, such as fruits, vegetables, grains, dairy products and meat. Organic farming practices are designed to encourage soil and water conservation and reduce pollution. Farmers who grow organic produce and meat don’t use conventional methods to fertilize, control weeds or prevent livestock disease. For example, rather than using chemical weedkillers, organic farmers may conduct more sophisticated crop rotations and spread mulch or manure to keep weeds at bay.

Here are some key differences between conventional farming and organic farming:



Apply chemical fertilizers to promote plant growth. Apply natural fertilizers, such as manure or compost, to feed soil and plants.
Spray synthetic insecticides to reduce pests and disease. Spray pesticides from natural sources; use beneficial insects and birds, mating disruption or traps to reduce pests and disease.
Use synthetic herbicides to manage weeds. Use environmentally-generated plant-killing compounds; rotate crops, till, hand weed or mulch to manage weeds.
Give animals antibiotics, growth hormones and medications to prevent disease and spur growth. Give animals organic feed and allow them access to the outdoors. Use preventive measures — such as rotational grazing, a balanced diet and clean housing — to help minimize disease.

Organic or not? Check the label

The U.S. Department of Agriculture (USDA) has established an organic certification program that requires all organic foods to meet strict government standards. These standards regulate how such foods are grown, handled and processed.

Any product labeled as organic must be USDA certified. Only producers who sell less than $5,000 a year in organic foods are exempt from this certification; however, they’re still required to follow the USDA’s standards for organic foods.

If a food bears a USDA Organic label, it means it’s produced and processed according to the USDA standards. The seal is voluntary, but many organic producers use it.

Products that are completely organic — such as fruits, vegetables, eggs or other single-ingredient foods — are labeled 100 percent organic and can carry the USDA seal.

Foods that have more than one ingredient, such as breakfast cereal, can use the USDA organic seal plus the following wording, depending on the number of organic ingredients:

  • 100 percent organic. To use this phrase, products must be either completely organic or made of all organic ingredients.
  • Organic. Products must be at least 95 percent organic to use this term.

Products that contain at least 70 percent organic ingredients may say “made with organic ingredients” on the label, but may not use the seal. Foods containing less than 70 percent organic ingredients can’t use the seal or the word “organic” on their product labels. They can include the organic items in their ingredient list, however.

Do ‘organic’ and ‘natural’ mean the same thing?

No, “natural” and “organic” are not interchangeable terms. You may see “natural” and other terms such as “all natural,” “free-range” or “hormone-free” on food labels. These descriptions must be truthful, but don’t confuse them with the term “organic.” Only foods that are grown and processed according to USDA organic standards can be labeled organic.

Organic food: Is it more nutritious?

The answer isn’t yet clear. A recent study examined the past 50 years’ worth of scientific articles about the nutrient content of organic and conventional foods. The researchers concluded that organically and conventionally produced foodstuffs are comparable in their nutrient content. Research in this area is ongoing.

Organic food: Other considerations

Many factors influence the decision to choose organic food. Some people choose organic food because they prefer the taste. Yet others opt for organic because of concerns such as:

  • Pesticides. Conventional growers use pesticides to protect their crops from molds, insects and diseases. When farmers spray pesticides, this can leave residue on produce. Some people buy organic food to limit their exposure to these residues. According to the USDA, organic produce carries significantly fewer pesticide residues than does conventional produce. However, residues on most products — both organic and nonorganic — don’t exceed government safety thresholds.
  • Food additives. Organic regulations ban or severely restrict the use of food additives, processing aids (substances used during processing, but not added directly to food) and fortifying agents commonly used in nonorganic foods, including preservatives, artificial sweeteners, colorings and flavorings, and monosodium glutamate.
  • Environment. Some people buy organic food for environmental reasons. Organic farming practices are designed to benefit the environment by reducing pollution and conserving water and soil quality.

Are there downsides to buying organic?

One common concern with organic food is cost. Organic foods typically cost more than do their conventional counterparts. Higher prices are due, in part, to more expensive farming practices.

Because organic fruits and vegetables aren’t treated with waxes or preservatives, they may spoil faster. Also, some organic produce may look less than perfect — odd shapes, varying colors or smaller sizes. However, organic foods must meet the same quality and safety standards as those of conventional foods.

Food safety tips

Whether you go totally organic or opt to mix conventional and organic foods, be sure to keep these tips in mind:

  • Select a variety of foods from a variety of sources. This will give you a better mix of nutrients and reduce your likelihood of exposure to a single pesticide.
  • Buy fruits and vegetables in season when possible. To get the freshest produce, ask your grocer what day new produce arrives. Or check your local farmers market.
  • Read food labels carefully. Just because a product says it’s organic or contains organic ingredients doesn’t necessarily mean it’s a healthier alternative. Some organic products may still be high in sugar, salt, fat or calories.
  • Wash and scrub fresh fruits and vegetables thoroughly under running water. Washing helps remove dirt, bacteria and traces of chemicals from the surface of fruits and vegetables. Not all pesticide residues can be removed by washing, though. You can also peel fruits and vegetables, but peeling can mean losing some fiber and nutrients.


  • Source: Mayo clinic house call

The Measurement of Lipids Currently and 9 Years Ago—Which Is More Associated With Carotid Intima-Media Thickness?

Massive evidence supports that increase of lipids bring more risk of atherosclerosis. However, it is not clear if lipids measured a long time ago bear more risk than the current measurement.


Lipids measured currently is more associated with carotid atherosclerosis than lipids measured long time ago.


A cohort of 1195 participants age 35 to 64 years was examined in both 1993–1994 and 2002 for serum lipids, and in 2002 for carotid intima-media thickness (CIMT) with B mode ultrasound. The associations of lipids at baseline and at reexamination with CIMT were analyzed and compared using multiple linear regressions.


All lipid variables, except for high-density lipoprotein cholesterol (HDL-C) both at baseline and reexamination, were significantly associated with age-adjusted CIMT in both males and females (all Ptrend <0.01). The age-adjusted mean of CIMT in all of the population was 0.696 mm in those having low low-density lipoprotein cholesterol (LDL-C) at both examinations, 0.719 mm in those having high LDL-C only at baseline, 0.706 mm in those having high LDL-C only at reexamination, and 0.727 mm in those having high LDL-C at both examinations. Further analysis showed that lipids measured at baseline remained significant, whereas lipids at reexamination became not significant in all models, except those for HDL-C and total cholesterol (TC)/HDL-C, which allow the lipids at different times to compete in association with CIMT.


Both the current measurement of lipids (TC, LDL-C, non-HDL-C, TC/HDL-C, and LDL-C/HDL-C) and the measurement from 9 years ago are significantly associated with CIMT, but the measurement from 9 years ago had an even stronger association.

Source: http://onlinelibrary.wiley.com





IGT ups risk for abnormal retinal vascular reactivity CVD.

Researchers in the United Kingdom have found a link between impaired glucose tolerance and microvascular and macrovascular function, as well as a direct association between retinal microcirculatory changes and established plasma markers for cardiovascular disease.

Sunni R. Patel, PhD, a postdoctoral fellow at University Health Network in Toronto and former researcher for the Vascular Research Laboratory and Ophthalmic Research Group at the School of Life and Health Sciences at Aston University in Birmingham, United Kingdom, and colleagues conducted a study involving 60 age- and sex-matched white European adults, 30 with IGT and 30 with normal glucose tolerance.

Patients with IGT had higher blood pressure values (P<.001), fasting triglyceride levels and triglyceride-to-HDL ratios (P<.001) vs. patients with normal glucose tolerance. According to data, blood glutathione levels were lower (reduced glutathione, P<.001; glutathione disulfide, P=.039; and total glutathione, P<.001), whereas plasma von Willebrand factor was increased in patients with IGT when compared with the control group (P=.014).

Moreover, patients with IGT displayed higher intima-media thickness in the right (P=.017) and left carotid arteries (P=.005) and larger brachial artery diameter (P=.015). Patients with IGT also had lower flow-mediated dilation percentage (P=.026) and glyceryl trinitrate-induced dilation (P=.012) than healthy control patients.

“The results of our pilot study suggest that IGT individuals demonstrate signs of early vascular dysfunction as measured by functional (at macro- and microcirculatory levels) and circulatory markers. Moreover, in addition to a relationship between functional macro- and microvascular parameters, there appears to be a direct correlation between the observed retinal microcirculatory changes and established plasma markers for CVD risk,” the researchers wrote.

Due to these observations, researchers wrote that there should be a possible emphasis on early CV screenings and interventions for those with a prediabetes diagnosis, including those with IGT.

“Retinal vascular imaging could emerge as a possible future option for individual risk stratification in diseased patients but also in individuals at risk for metabolic and CV pathologies,” the researchers wrote.

Source: Endocrine Today.



Bone formation markers increase from olive oil, Mediterranean diet in the elderly.

The consumption of virgin olive oil as part of a Mediterranean diet may protect against bone loss in the elderly, according to Spanish researchers.

In a 2-year randomized, controlled trial of 127 men aged 55 years to 80 years, researchers concluded that olive oil increases the body’s concentration of the serum osteocalcin, which protects the bone. Participants had no prior history of cardiovascular disease, but had either type 2 diabetes or at least three risk factors for developing the disease, including family history, hypertension and dyslipidemia.

“The intake of olive oil has been related to the prevention of osteoporosis in experimental and in vitro models,” José Manuel Fernández-Real, MD, PhD, lead author from the Hospital Dr. Josep Trueta in Girona, Spain, stated in a press release. “This is the first randomized study which demonstrates that olive oil preserves bone, at least as inferred by circulating bone markers, in humans.”

This study was published ahead of print in the Journal of Clinical Endocrinology and Metabolism.

Fernández-Real and colleagues also measured HDL-cholesterol, total cholesterol, glucose and triglycerides at baseline in addition to osteocalcin, but only olive oil as well as a Mediterranean diet proved to increase levels of osteocalcin and other bone formation markers in the body.

In the release, Fernández-Real noted that osteocalcin in the body has other effects, such as increasing insulin secretion, in addition to protecting bone.

“It is important to note that circulating osteocalcin was associated with preserved insulin secretion in subjects taking olive oil,” Fernández-Real stated. “Osteocalcin has also been described to increase insulin secretion in experimental models.”


Fernández-Real JM, Bulló M, Moreno-Navarrete JM, et al. A Mediterranean diet enriched with olive oil is associated with higher serum total osteocalcin levels in elderly men at high cardiovascular risk. J Clin Endocrinol Metab. 2012 Aug 1. Epub ahead of print.

Source: Endocrine Today.