A Cold Of The Soul

In Japan, like the USA, pharmaceutical companies push over-medication.  See this article, abstract:

In Japan, depression provides the most drastic example of the impact of disease awareness campaigns. Until the late 1990 s, the public's attitude toward depression was generally unfavorable, due to the negative connotations of the Japanese word for clinical depression, 'utsubyou'. After the 1999 introduction of the first selective serotonin re-uptake inhibitor, pharmaceutical companies initiated educational campaigns. In order to aid the drug's acceptance, they coined the catchphrase 'kokoro no kaze', which literally means 'a cold of the soul'. Thanks to these marketing practices, antidepressant sales have increased six fold, from ¥ 14.5 billion in 1998 to ¥ 87 billion in 2006. However, the catchphrase 'kokoro no kaze' masked a critical difference between a cold and depression. It falsified the nature of treatment for depression by concealing the putative duration of medication. Owing to this distortion of information, pharmaceutical companies were assured a steady stream of profits. Now, the pharmaceutical industry is shifting its focus from depression to bipolar disorder. Japanese psychiatrists can learn a great deal from their experience with the aggressive marketing of antidepressants. In the case of depression, over-medication arguably did more harm than good. The same risk exists with other conditions, including bipolar disorder.

Sound familiar?  Now, if medication is necessary, take it.  I do.  But take medication that is necessary, as determined by your physician, your own research, and the cooperation between yourself and your health care team. Talk to your physician, and do research.  Medication solely to boost pharmaceutical profits is not the way to go.  Good medications are saviors, antibiotics have saved millions of lives, and we should not reject biomedical advances.  But the Japanese case outlined here describe a case where unnecessary overmedication has taken place.  One must understand the difference.

Anti-Epileptic Drugs And Bone Loss

Drugs against epilepsy can cause bone loss, particularly in post-menopausal women.  A study in rats demonstrated that this is due to changes in Wnt signaling and this effect was especially pronounced in ovariectomised rats, showing that estrogen loss from menopause can enhance the problem. Abstract:

Secondary osteoporosis is the major concern associated with long term intake of antiepileptic drugs (AEDs). Women are the vulnerable targets owing to post-menopausal bone loss. In the present work, we evaluated the effect of 10 weeks of treatment with AED therapy (carbamazepine, CBZ, 75 mg/kg; sodium valproate, SVP, 300 mg/kg; levetiracetam, LTM, 150 mg/kg) on bone mineral density and microarchitecture at femoral epiphysis, lumbar vertebrae and proximal tibia of normal and ovariectomised Wistar rats. In addition, we measured serum levels of vitamin D, receptor activator of nuclear factor kappa β-ligand (RANKL), procollagen type 1 amino-terminal propeptide (P1NP) and wnt inhibitors (sclerostin and DKK-1) following AED therapy. Micro-computed tomography analysis of bones revealed significant reduction in BMD at femur epiphysis and lumbar vertebrae with all the three AEDs evaluated. At proximal tibia, only CBZ showed a significant decline. The reduction in BMD was more pronounced in ovariectomised rats. AEDs also resulted in alteration of micro-CT parameters. These changes were accompanied by an increased serum RANKL with all AEDs while vitamin D levels were reduced only with CBZ treatment and P1NP levels were reduced with SVP and CBZ. Serum sclerostin levels were elevated following all AEDs in normal and ovariectomised rats except with CBZ in normal rats. However, increase in DKK-1 levels was observed with only LTM. Ovariectomy itself resulted in increased RANKL, sclerostin and DKK-1 and reduced vitamin D and P1NP levels. Significant differences were discernible between normal and ovariectomised rats treated with AEDs in all the parameters. However, while sclerostin increased further upon AEDs treatment, P1NP decreased with SVP and CBZ and serum DKK-1 levels showed a declining trend with all the three AEDs studied. We confirm adverse effects on bone following AEDs in female rats. Further, our results demonstrate for the first time that these effects are more pronounced in ovariectomised rats as compared to normal rats and that this could be related to estrogen deficiency which in turn enhances bone resorption via increased RANKL and reduces bone formation via increased sclerostin and reduced P1NP. Finally, our study demonstrated for the first time that AED treatment displayed changes in the serum levels of wnt inhibitors and hence modulation of wnt inhibitors might be partly involved in their adverse effects on bone.

Drugging Test Anxiety?

I suppose this can be the next grand adventure in “learning disability” pharmaceutical adjustments: taking drugs for “test anxiety.”  At some point people need to be able to get through life without being medicated for every stressful scenario unfolding in their lives.  Abstract:

Test anxiety is severely disabling to students whose fear of examinations causes cognitive dysfunction that paralyzes their thinking the way stage fright impairs actors ability to act. In studies using subjective evaluations among actors and musicians, beta-blockade relieved stage fright and has been used informally to treat test anxiety in students without objective measures of effectiveness. The Scholastic Aptitude Test (SAT) was chosen as an objective test instrument to confirm the effect of beta-blockade on test anxiety and performance. Thirty-two high school students who had already taken the SAT before enrolling in this study and who had stress-induced cognitive dysfunction on exams were given 40 mg of propranolol one hour before they retook those tests. Mean SAT scores with beta-blockade were 130 points higher than on the initial SAT done before entering the study without medication (p = less than .01). A single dose of propranolol immediately before the SAT permitted improved performance in students prone to cognitive dysfunction due to test anxiety.

Repurposing Old Drugs For New Roles

Here is an interesting article about expanding the use of old, approved drugs for new purposes.  In theory, this is a good idea, since the safety profile of the drug and its various side effects would already be known, and sometimes “side effects” can mean the drug can be useful against other disorders than originally intended.  However, this requires additional testing to determine if the drug is actually effective in the new role for which it is being proposed. The problem is that when you consider expensive drugs still under patent, pharmaceutical companies have a patent incentive to do such testing, but not for low-cost generic drugs. The author proposes some ways around this: government funding, prize funds, leveraging existing data.  Given the cost of new drugs and the uncertainty of side effects, particularly long-term side effects, once they are in clinical use, repurposing old drugs has promise in being more safe and efficient.  From the article:

US Food and Drug Administration (FDA) approval of a new drug typically coincides with a period of patent protection, during which the manufacturer will often apply for additional indications to expand the market for the product. For example, the tyrosine kinase inhibitor imatinib (Gleevec; Novartis) was originally approved to treat Philadelphia chromosome–positive chronic myelogenous leukemia, but has since been approved for treatment of other cancers. Many noncancer drugs also follow this pattern, including botulinum toxin A (Botox; Allergan), which was originally approved for the treatment of strabismus and blepharospasm and subsequently approved for treatment of cervical dystonia, cosmetic uses, and chronic migraine.

This pattern of additional testing and approvals is common for more expensive on-patent drugs, but new indications are rarely sought for less-expensive generic drugs, for which it is more difficult to profit from the research. This creates a policy conundrum: follow-on innovation for low-cost generic products offers a rare opportunity to simultaneously improve health outcomes and likely reduce health care expenditures, but how could such research be encouraged?

Big Pharma Disease Mongering?

Can’t say I’m surprised by this.  Related to that, if you work in an academic setting, you'll find plenty of students who suddenly are able to find a health care professional to diagnose them with a "learning disability" requiring "accommodation" (and medication - amphetamine stimulants - in many cases) once they fail some classes.  Interestingly, the same students who were straight-A students as college undergraduates mysteriously develop a "learning disability" in their early-mid 20s (or later) once they have problems with difficult courses in some sort of post-graduate education.

The pharmaceutical industry’s image has been significantly damaged in recent years as the public discovered the role its aggressive marketing played in fueling the opioid epidemic. But the American people are still largely in the dark about what may be pharma’s most effective tactic for pushing drugs — marketing diseases.

There’s a substantial body of medical literature dating back to the early ’90s about the practice known as “disease mongering.” Pharmaceutical companies regularly pathologize everyday experiences, convince doctors that they are serious problems, tell a hypochondriacal public it needs help and offers the cure: a new drug. Against the onslaught of billions of dollars in marketing campaigns each year, however, researchers’ warnings about these tactics have gone largely unheeded…

 …“Marketing for a drug can start seven to 10 years before they go on the market. Because it’s illegal to promote a drug before it goes on the market, what they’re promoting is the disease. That’s not illegal to do because there’s no regulation on creating diseases,” Fugh-Berman told Yahoo News.

Lisa Schwartz and Steven Woloshin, co-directors of the Center for Medicine and Media at Dartmouth Institute for Health Policy and Clinical Practice, said disease-awareness campaigns may seem caring or educational but are often just marketing in disguise. The campaigns often follow three basic steps: lower the bar for diagnosis, raise the stakes so people want to get tested and spin the evidence about a drug’s benefits and risks. These steps were seen in campaigns on testosterone deficiency, bipolar disorder and restless leg syndrome…

…Fugh-Berman recalled taking an online test with her coworkers at PharmedOut, a group she directs at Georgetown that exposes pharmaceutical marketing and promotes evidence-based prescribing. The test on pseudobulbar affect (PBA), which manifests when specific brain damage leads to laughing or crying that is inappropriate and unconnected to a person’s emotions, suggested that normal human expressions could be signs of PBA with questions like “Do you ever find things funny that other people don’t find funny?” and “Do you cry easily?”

“Almost every woman failed. Only one woman passed. Most of the men failed, but more of them passed. I would say that anyone who passed the test I was actually worried about,” Fugh-Berman said…

… “I feel that there are people involved in creating new diseases and promoting drugs that aren’t really needed who are pretty amoral. Their measurement of success for themselves is strictly sales,” Pearson said. “There are good-spirited and good-hearted people in companies who are proud of developing something that provides help to some people — and then their marketing department gets ahold of it and turns it into something else.”

Clinical Benefits Of Marijuana?

Please note that this blog does not take sides in the legalization debate, and certainly does not condone or promote illegal drug use in any way, but is presenting this study for information purposes only. Legal clinical use  of such drugs should strictly be under a physician's supervision. Abstract:

BACKGROUND:

Numerous physical, psychological, and emotional benefits have been attributed to marijuana since its first reported use in 2,600 BC in a Chinese pharmacopoeia. The phytocannabinoids, cannabidiol (CBD), and delta-9-tetrahydrocannabinol (Δ9-THC) are the most studied extracts from cannabis sativa subspecies hemp and marijuana. CBD and Δ9-THC interact uniquely with the endocannabinoid system (ECS). Through direct and indirect actions, intrinsic endocannabinoids and plant-based phytocannabinoids modulate and influence a variety of physiological systems influenced by the ECS.

METHODS:

In 1980, Cunha et al. reported anticonvulsant benefits in 7/8 subjects with medically uncontrolled epilepsy using marijuana extracts in a phase I clinical trial. Since then neurological applications have been the major focus of renewed research using medical marijuana and phytocannabinoid extracts.

RESULTS:

Recent neurological uses include adjunctive treatment for malignant brain tumors, Parkinson's disease, Alzheimer's disease, multiple sclerosis, neuropathic pain, and the childhood seizure disorders Lennox-Gastaut and Dravet syndromes. In addition, psychiatric and mood disorders, such as schizophrenia, anxiety, depression, addiction, postconcussion syndrome, and posttraumatic stress disorders are being studied using phytocannabinoids.

CONCLUSIONS:

In this review we will provide animal and human research data on the current clinical neurological uses for CBD individually and in combination with Δ9-THC. We will emphasize the neuroprotective, antiinflammatory, and immunomodulatory benefits of phytocannabinoids and their applications in various clinical syndromes.

Olanzapine Side Effects And Wnt Signaling

Many drugs have unintended side effects.  A perfect example of this is weight gain and insulin resistance (metabolic syndrome characteristics) resulting from use of the antipsychotic drug olanzapine.  Aberrant Wnt signaling is associated with these effects, which can be reversed (in mice) by metformin (which of course has its own set of side effects; we are at a point in which people will be on sets of medications, some of which are to reverse the side effects of other medications). Abstract:

Olanzapine is a widely used atypical antipsychotic medication for treatment of schizophrenia and is often associated with serious metabolic abnormalities including weight gain and impaired glucose tolerance. These metabolic side effects are severe clinical problems but the underpinning mechanism remains poorly understood. Recently, growing evidence suggests that Wnt signaling pathway has a critical role in the pathogenesis of schizophrenia and molecular cascades of antipsychotics action, of which Wnt signaling pathway key effector TCF7L2 is strongly associated with glucose homeostasis. In this study, we aim to explore the characteristics of metabolic disturbance induced by olanzapine and to elucidate the role of TCF7L2 in this process. C57BL/6 mice were subject to olanzapine (4 mg/kg/day), or olanzapine plus metformin (150 mg/kg/day), or saline, respectively, for 8 weeks. Metabolic indices and TCF7L2 expression levels in liver, skeletal muscle, adipose, and pancreatic tissues were closely monitored. Olanzapine challenge induced remarkably increased body weight, fasting insulin, homeostasis model assessment-insulin resistance index, and TCF7L2 protein expression in liver, skeletal muscle, and adipose tissues. Notably, these effects could be effectively ameliorated by metformin. In addition, we found that olanzapine-induced body weight gain and insulin resistance actively influence the expression of TCF7L2 in liver and skeletal muscle, and elevated level of insulin determines the increased expression of TCF7L2 in adipose tissue. Our results demonstrate that TCF7L2 participates in olanzapine-induced metabolic disturbance, which presents a novel mechanism for olanzapine-induced metabolic disturbance and a potential therapeutic target to prevent the associated metabolic side effects.

Exercise As An Anti-Depressant

Regular exercise can reduce depressive symptoms to an extent that can mimic chronic antidepressant treatment (of course, one likely won’t hear about this from most doctors or from the pharmaceutical companies pushing their samples onto those doctors), and there are molecular mechanisms for this, apparently involving the Wnt signaling pathway. Abstract:

Regular exercise reduces depressive-like behavior activation. In this study, we look for exact roles of exercise on molecular and neuronal mechanisms for antidepressant action by studying the hippocampal neuroplasticity and proliferation. Increased hippocampal neurogenesis with exercise has potential significance for depression. Exercise promotes brain health in the molecular levels in the hippocampus and also affects behavior in a similar way to chronic antidepressant treatment. Wingless (Wnt) and frizzled signaling system plays an important role in cell proliferation, growth, and differentiation during development. Our results demonstrate complicated, differential effects of antidepressants on Wnt signaling system, and assume a role for selected signaling molecules in the neurogenic activity of antidepressant care. Our review suggests that exercise may preserve brain function by increasing neurogenesis through activating Wnt signaling pathway in the psychiatric disorders, such as depression.

Maybe exercise rather than popping pills should be the first line treatment for many mental, as well as more directly physical, disorders?  First, ask you doctor about it - an informed doctor - and follow his or her advice.  Everyone is different.  Some people may require medication, others may only need exercise.  Get the medical consultation you require to figure out which category you may be in, if you require such help.

Drugs And The Gut Microbiota

Non-antibiotic drugs can alter the gut microbiota. Given the profound effects that microbiota can have on human health and behavior, one wonders whether any of the effects or, especially and likely, side-effects of these drugs is at least partially due to disruption of the intestinal ecology. Abstract:

A few commonly used non-antibiotic drugs have recently been associated with changes in gut microbiome composition, but the extent of this phenomenon is unknown. Here, we screened more than 1,000 marketed drugs against 40 representative gut bacterial strains, and found that 24% of the drugs with human targets, including members of all therapeutic classes, inhibited the growth of at least one strain in vitro. Particular classes, such as the chemically diverse antipsychotics, were overrepresented in this group. The effects of human-targeted drugs on gut bacteria are reflected on their antibiotic-like side effects in humans and are concordant with existing human cohort studies. Susceptibility to antibiotics and human-targeted drugs correlates across bacterial species, suggesting common resistance mechanisms, which we verified for some drugs. The potential risk of non-antibiotics promoting antibiotic resistance warrants further exploration. Our results provide a resource for future research on drug-microbiome interactions, opening new paths for side effect control and drug repurposing, and broadening our view of antibiotic resistance.

Serotonergic Psychedelics And Personality

For general interest, abstract:

Serotonergic psychedelics act as agonists at cortical 5-HT2A receptors and seem to induce personality changes. We conducted a systematic review of studies assessing the effects of these drugs on personality. Papers published from 1985-2016 were included from PubMed, LILACS, and SciELO databases. Three hundred and sixty-nine studies were identified, and 18 were included. Specific personality traits, such as Absorption and Self-Transcendence, seem to influence the effects of psychedelics, and psychedelic drug users and nonusers appear to differ in some personality traits. Psychedelics administered in controlled settings may induce personality changes, such as increased Openness and Self-Transcendence. Increases in global brain entropy induced by acute psychedelic administration predicted changes in Openness, and Self-Transcendence was negatively correlated with cortical thinning of the posterior cingulate cortex in long-term religious ayahuasca users. Acute and long-term use of psychedelics is associated with personality changes that appear to be modulated by 5-HT2A receptors. These changes seem to induce therapeutic effects that should be further explored in randomized controlled studies.

Leaf Extract Against Colorectal cancer

Here is a study suggesting that Ginkgo biloba L. leaf extract may be beneficial against colorectal cancer by affecting important cell signaling pathways that mediate that disease. The authors state: “The outcomes of the present investigation encourage the use of Ginkgo biloba L. leaf extract as a complementary and alternative therapeutic approach to abate CRC.”  As always consult your own physician; in my opinion, “complementary” may be useful, but “alternative” (as in use this but do not use traditional medical treatments) is a mistake. I have heard of too many horror stories of patients eschewing regular treatment for alternatives and then dying if a curable cancer because they realized, too late, that the alternative was really no alternative at all.  But, again, I am not a medical doctor and I am only giving my own opinion based on scientific background as well as personal experience and anecdote.  I would urge all cancer patients to follow the advice of their oncologists and, of course, ask whether other things can complement treatment.

Exercise Instead Of Drugs For Knee Osteoarthritis

It should come as no surprise of readers of this blog that quadriceps (muscles of the front of the thigh) exercise can as effective as nonsteroidal anti-inflammatory drugs against knee osteoarthritis.  And yet, taking pills is the “default” for the medical profession – everything “solved” with drugs.  Abstract:

OBJECTIVES:

To examine the effect of home-based exercise on knee osteoarthritis among Japanese in comparison with that of nonsteroidal antiinflammatory drugs (NSAIDs).

DESIGN:

An open-labeled, randomized, controlled, multiclinic trial compared home-based quadriceps exercise with NSAIDs. Treatments were basically evaluated after 8 wks and compared with the baseline scores. Outcomes were evaluated with a set of psychometric measurements including the Western Ontario and McMaster Universities Arthritis Index (WOMAC), 36-Item Short-Form Health Survey (SF-36), Japanese Knee Osteoarthritis Measure (JKOM), and pain with the visual analog scale.

RESULTS:

A total of 142 patients entered this trial to provide the baseline data. After 21 cases withdrew, the final number analyzed was 121 cases: 63 for the exercise group and 58 for the NSAIDs group. Between these two groups, there was no significant difference in gender, age, body height and weight, body mass index, or each score at baseline. The subjects in both groups showed improvements in all scores at the end of intervention. The difference in improvement rate of each score between the two groups was not statistically significant, though the mean rank score measured with JKOM in the exercise was slightly better than that of the NSAIDs.

CONCLUSIONS:

Home-based exercise using quadriceps strengthening improves knee osteoarthritis no less than NSAIDs.

The FDA And Vasopressin

The FDA got involved in trying to regulate marketed previously unapproved drugs, with results perhaps not unexpected to those of us who have taken a MBA-level course in economics.  From the (publicly available) paper linked above:

In May 2017, the US Food and Drug Administration (FDA) announced a Drug Competition Action Plan, designed to address competition and pricing in the generic market and improve access to prescription drugs. One of FDA’s stated goals is to reexamine “places where its rules—including standards and procedures related to generic drug approvals—are being used in ways that may create obstacles to generic access,” instead of ensuring the vigorous competition Congress intended. In this Viewpoint, we examine FDA’s 2006 Unapproved Drugs Initiative (UDI), designed to strengthen the agency’s regulatory oversight related to unapproved marketed drugs. Using an illustrative example, we discuss this initiative’s unintended consequences, as it appears to have created obstacles to generic drug access, likely increasing prescription drug costs…On November 14, 2014, Par received FDA approval for Vasostrict, and on December 15, 2014, FDA instructed all other suppliers of unapproved intravenous vasopressin to stop manufacturing their products by January 30, 2015, leaving only Par with a marketed product. Subsequently, the average wholesale price of intravenous vasopressin increased from $4.27 to $138.40 per vial in November 2016, a 3141% increase. In 2013, when there were multiple competing suppliers, total sales from intravenous vasopressin approximated $4 million. As of November 2016, Vasostrict achieved annualized sales of nearly $400 million. As a result of the high cost, reports have surfaced of vasopressin being removed from code carts, making it unavailable in life-threatening situations.

I’ll leave it to the reader to ponder whether the vast increase per vial price for vasopressin was a justifiable change, and whether the unavailability of this drug for endangered patients is somehow compatible with the FDA’s ostensible mission.

The FDA and Big Pharm: a match made in heaven…or hell.  You decide.  Look at the facts reported in the paper and the other link and ponder well.

Another Drug For Cardiovascular Disease

A report on the effectiveness of another drug for cardiovascular disease is found here.  I would like to see more on lifestyle (e.g., diet and exercise) however.  Abstract:

Background Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. Methods We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. Results During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. Conclusions Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .).

Diet Vs. Drugs

In general, I believe that, when and where appropriate, lifestyle changes should be tried first before taking drugs to deal with certain common types of chronic metabolic disorders (but of course always consult with your physician, as "in general" does not apply to every specific case). The experts agree with my opinion:

Many Americans, when faced with a serious health risk like high cholesterol, opt to take a pill rather than adopt healthier living habits.

A middle-aged woman I know is typifies this attitude. Thrilled with how well medication has controlled her rising cholesterol level, she continues to indulge in foods rich in cholesterol-raising saturated fats. She also carries around more body fat, especially risky abdominal fat, than is considered healthful.

I met people like that. For example, some people with Type II Diabetes believe that taking medication gives them green light to load up with cookies, cakes, and doughnuts.

Dr. Philip Greenland, a cardiologist and epidemiologist at Northwestern University Feinberg School of Medicine, said, “People should be following a heart-healthy diet, keeping their weight under control and exercising regularly. This would be a highly preferable approach. Unfortunately, it’s not the direction we’re going in.”

Admittedly, swallowing a little pill every day is simpler than changing one’s behaviors — and especially one’s eating habits. Yet experts like Dr. Greenland say that even when taking a statin or some other cholesterol-lowering drug, changes in diet and exercise habits are needed to maximize the drug’s benefits. He and others insist that drugs should be a last resort, after lifestyle changes fail to lower serum cholesterol adequately.

I agree. Unfortunately, Dr. Greenland is correct that this is not the direction we are going on. Everything and everyone needs to be medicated, it seems. I recently read a suggestion stating that drugs for treating the consequences of obesity are needed, since it is unrealistic to think people are going to lose weight. In other words, eat excessively, be obese, and then take a pill to try and evade the consequences. Of course, all of these drugs have side effects.  Wouldn’t it be easier to attack the problem rather than its consequences?  Lifestyle changes involving diet and exercise may help the underlying problem, and do so without expensive medications and their side-effects.

Noting that “every food a person might eat either fights or contributes to disease,” Dr. Kopecky said his clinic “tries to get everyone on a Mediterranean diet,” the traditional eating habits of people living in Greece and southern Italy. In addition to its heart benefits, studies suggest the Mediterranean diet may “reduce the risk of Alzheimer’s disease, cancer, Parkinson’s disease, diabetes, arthritis and the metabolic syndrome”… “people in Greece eat an average of nine servings a day of antioxidant-rich fruits and vegetables,” and the booklet outlines a long list of potentially healthful foods. Some examples include prunes, blueberries, red grapes, oranges, strawberries, kale, spinach, brussels sprouts, broccoli, beets, red bell peppers, corn and eggplant.

At a minimum, Americans should strive to consume two or more servings of vegetables and two to three or more servings of fresh fruit each day. If “fresh” is not available, “fresh frozen” is the next best option.

Living near the sea, Mediterraneans eat lots of seafood, often daily, and the Mayo diet recommends three or more servings a week of fish or shellfish. One or more servings should be a fatty fish rich in protective fish oils, like salmon, tuna, bluefish, sardines, mackerel and trout.

The white meat of chicken or turkey, eaten without the skin, is the land animal protein of choice, the Mayo Clinic says, with a serving size limited to 3 ounces of cooked meat, about the size of a deck of cards.

Unlike many Americans, people living along the Mediterranean also consume lots of foods with vegetable protein: legumes like split peas, lentils and peanuts, and beans like lima, black, red, kidney and navy…Whole grain breads and cereals are part of the recommended diet, but note that a serving of bread is one slice. Breads should be eaten plain or dipped in olive oil, the Mayo booklet says.

Which brings us back to fats. Olive oil, especially extra-virgin and virgin, the least processed forms, or canola oil should be used in place of butter or margarine…Eggs are back in fashion, consumed in moderation. That means a limit of three to four egg yolks a week, though no limit on egg whites. A good trick when preparing an omelet or scrambled eggs is to use two egg whites for every one yolk…However, red and processed meats should be limited to one three-ounce serving a week. And those cherished treats and desserts — pastries, cakes, doughnuts, cookies, pudding, French fries, potato chips and all sweetened and diet carbonated soft drinks — are best avoided altogether…Likewise, avoid high-fat dairy products…

Of course, what you eat is only half of the health-saving story. Regular physical exercise is a critical ingredient, even if it doesn’t result in weight loss. “Fitness trumps fatness,” Dr. Kopecky said, adding that being fit even while remaining fat markedly reduces cardiovascular risk. He urges parents to establish heart-healthy habits early in their children’s lives. “Patterns for physical activity are set by ages 6 to 9, and healthy eating habits by ages 9 to 12; together, they can result in a much lower risk for developing heart disease as adults,” he said.

This is all sound advice. If radical changes are considered too difficult at first, then go slowly. Reduce rather than eliminate the more unhealthy foods and continue to reduce their intake over time, until they are eliminated or are taken at a reasonable and acceptable frequency. Gradually increase your intake of fruits, vegetables, and whole grains. Increasingly incorporate physical activity into your daily regimen. Over time, you will have reached the required goals and objectives.

Conservative Antibiotic Use is Prudent

The over-prescription, over-use, and wrong-use of antibiotics have helped fuel the epidemic of antibiotic resistance. Less, more conservative use of these drugs would be prudent. Using antibiotics when they are not needed not only fuels resistance, but is costly and can have a negative impact on the normal human bacterial microbiome. In general, all medications should be used appropriately and not indiscriminately used in cases where there would be little to no benefit (or even harm).

For uncomplicated respiratory infections, strategies that delay the patient’s pick-up or use of antibiotics can result in less antibiotic use with equal satisfaction, according to a new study.

Patients who had to go pick up their prescriptions from the primary care office or who delayed taking the antibiotics experienced slightly greater symptoms for a slightly longer time during their illness than people who got antibiotics immediately, but all groups had similar satisfaction levels.

Most respiratory infections, like pharyngitis or bronchitis, are caused by viruses, not bacteria, and antibiotics do not modify the infections significantly. But most patients with symptoms of these infections still receive an antibiotic in the U.S., the authors write.

Using antibiotics when they do little to help puts the patient at risk of unnecessary side effects and helps make the targeted bacteria resistant to the drugs.

BOOST YOUR BRAIN: SKIP THE DRUGS, EXERCISE INSTEAD

He has done it again. 

The anonymous author of the YouTube channel What I've Learned has uploaded another brilliant video. This time it is on exercise and what exercise does for your brain, WHY Exercise is so Underrated (Brain Power & Movement Link).
 
I would suggest that you also check the website of the author, as the transcripts of the What I've Learned videos are posted there.

For more information on the topic, read my previous post, Jumping jacks or medications. I recently re-read it, and I realized that I was naïve when advising my readers under Actionable, “Dear doctors, instead of ADHD medications, would you please prescribe jumping jacks to our children?”

Why is this naïve? Because the frightening truth is that your doctors might be on the same medications themselves. I have had numerous conversations with medical students who have seen the inner works of clinical practices and I assure you that not only the medical students, but also some of the young MDs are “enhancing” their everyday professional performance with drugs. 

Therefore, do not expect that the doctors will help you overcome your dependence on pharmaceuticals. You have to take care of yourself. The more you know about psychotropic drugs, the better you will protect yourself.