PRACTICAL POINTERS
PRIMARY CARE
“ME TOO” PRODUCTS—FRIEND OR FOE?
OMEGA 3 FATTY ACIDS AND CARDIOVASCULAR
DISEASE
MEMANTINE TREATMENT IN PATIENTS WITH
MODERATE TO SEVERE ALZHEIMER DISEASE
RISKS OF TESTOSTERONE-REPLACEMENT
THERAPY
HYPOGONADISM IN ELDERLY MEN—WHAT TO DO
UNTIL THE EVIDENCE COMES
HELICOBACTER PYLORI ERADICATION TO
PREVENT GASTRIC CANCER
FOLIC ACID AND THE PREVENTION OF
NEURAL TUBE DEFECTS
CORONARY ARTERY CALCIUM SCORE COMBINED
WITH FRAMINGHAM RISK SCORE
EFFECTS OF AN AD LIBITUM LOW-FAT,
HIGH-CARBOHYDRATE DIET
EFFECTS OF STRONTIUM IN WOMEN WITH
POSTMENOPAUSAL OSTEOPOROSIS
EFFICACY AND SAFETY OF LOW-DOSE
ASPIRIN IN POLYCYTHEMIA VERA
DAILY ASPIRIN—ONLY HALF THE ANSWER FOR
POLYCYTHEMIA VERA
“WAKEFULNESS ENHANCER” ROUSES CONCERN
SHOPPING ‘TIL WE DROP—WHAT IS WRONG
WITH IT?
ARCHIVES INTERNAL MEDICINE EDITED BY RICHARD T. JAMES JR. MD
ANNALS
INTERNAL MEDICINE 400
AVINGER LANE, SUITE 203
Rjames6556@aol.com DAVIDSON
N2 28036 USA
www.practicalpointers.org
The epidemic of childhood obesity has been attributed largely
to a decline in total energy expenditure (TEE).
This study postulated that the lifestyle of contemporary young children is
sedentary.
Levels of TEE were low at ages 3 and 5 in both sexes.
Lifestyles in this sample of youngsters were sedentary. This would increase
risk of obesity. Their total energy expenditure was significantly lower than
the UK estimate average requirement for energy for children.
Children typically spent only 20-25 min per day in
moderate to vigorous physical activity. Present recommendations are that they
should accumulate at least 60 min daily. “There is a widespread perception
among parents and health and educational professionals that young children are
spontaneously active. Actually, modern children establish a sedentary lifestyle
at an early age.”
Prevalence of childhood obesity has increased strikingly in
recent years.
The nature of human physiology is such that it is extremely
difficult, if not impossible, to maintain a healthy bodyweight with a low level
of physical activity.
Obesity arises from an imbalance in which energy intake
exceeds energy expenditure. This means that sedentary people must maintain a
low intake of energy to avoid obesity. Human physiology did not develop to
support restriction of energy intake. It is difficult for most people to do so
consistently over time
We have to teach children (and adults) to use their
intellect to push back against the environment. Such a change can be done by
eating a little less and being a little more physically active than ordinarily.
Small changes would counter the natural tendency to succumb to the environment.
“We suggest that weight gain in 90% of the US adult
population could be prevented by reducing positive energy balance by only 100
kcal per day.” Small and achievable changes in behavior can have a big impact.
Me-too products create competition among drug and device
manufacturers. Competition is a powerful driver for better quality and lower
costs. Health care leaders who struggle
to provide good care with limited resources see me-too products not as a
problem, but as an important part of the solution.
The first product in a new class defines the baseline value
equation. [Value = benefit / harm-cost] The manufacturer may set a high price
and may have no trouble selling the product at its asking price. When a second
product in the same class comes along, its manufacturers must offer a better
value. That product must lead to a better outcome or it must be less expensive.
For market forces to really work, physicians have to choose
products as if costs matter.
“If it were
not for the nicotine in tobacco, people would be little more inclined to smoke
than they are to blow bubbles.”
Experimenting with smoking usually begins in the early
teenage years. It is driven predominantly by psychosocial motives. Smoking a
cigarette is a symbolic act of rebellion, and a statement of independence. The desired image is sufficient for the
novice smoker to tolerate the aversion of the first few cigarettes, after which
the pharmacological factors assume much greater importance. As the force from
the psychological symbolism subsides, the pharmacological effect takes over to
sustain the habit. Absorption of nicotine from the lung and transfer to the
brain is almost instantaneous and complete.
Tolerance soon develops, and chronic users probably do
not obtain absolute improvements in performance, cognitive processing, or mood.
A plausible explanation for why smokers perceive cigarettes to be calming may
come from a consideration of the effects of nicotine withdrawal. Smokers start
to experience impairment of mood and performance within hours of their last
cigarette, and certainly overnight. These effects are completely alleviated by
smoking a cigarette.
“Early cessation is especially important.”
Omega 3 fatty acids (O3FA) from fish and fish oils can protect against coronary heart
disease (CHD). In this era of
polypharmacy, many persons believe that simple dietary interventions or
nutritional supplements may be a more natural and acceptable method of
providing benefits.
The American Heart Association recommends:
Patients without
documented CHD should eat a variety of fish (preferably oily) at least twice
weekly. Diet should also include vegetable oils.
Patients with
documented CHD should consume 1 g of O3FA and O6FA daily.
Physicians may prescribe 2-4 g/d of O3FA and O6FA
daily, provided as capsules, for patients with hypertriglyceridemia.
In October 2003, the FDA approved memantine (Namenda) for treatment of moderate to
severe AD. Memantine is a blocker of the receptor for aspartate. It is a new
class of drug.
This study hypothesized that adding memantine (Namenda) to donepezil (Aricept ) would result in clinical
benefit and would be well tolerated.
Memantine resulted in significant statistical, but
only slight clinical benefit when added to donepezil. It appeared safe.
Investigators, as in this report, often stress
statistically significant improvement, not clinical improvement. This may be
misleading. In my view, the outcome of this study is disappointing.. The
investigators place a spin on benefits by noting the statistically significant
outcomes. This may appear to be an impressive result, but it is not clinically
important.
Hypogonadism is a clinical condition in which low levels of
serum testosterone are found in association with specific signs and
symptoms: diminished libido and sense
of vitality, erectile dysfunction, , depression, anemia, and reduced muscle
mass and bone density. Prescriptions for testosterone supplementation have increased
substantially over the past decade.
Reports indicate that testosterone replacement may produce a
wide range of benefits: improvement in
libido, bone density, muscle mass, body composition, mood, erythropoiesis, and
cognition.
No studies have yet been initiated to assess benefits and
risks, especially possible stimulation of prostate cancer. But, “Despite
decades of research, there is no compelling evidence that testosterone has a
causative role in prostate cancer”. There is no compelling evidence to
suggest that men with higher testosterone levels are at greater risk of PC or
that treating men with hypogonadism with exogenous androgens increases risk.
Nevertheless, the authors advocate routine biopsy in all men presenting for
replacement therapy
Should primary care clinicians deal with this problem? Should
they refer patients seeking therapy to a urologist with considerable
experience? At the present stage of
development, I would follow the second course.
The value of a therapy has been described as: Value =
benefits
harms-costs
I believe the benefits are somewhat nebulous and unknown
long-term. Harms are potentially great. Cost is considerable considering
consultation and laboratory fees as well as the cost of the testosterone.
A long-awaited report from the Institute of Medicine (IOM)
concluded that there is insufficient evidence that testosterone benefits
elderly men.
Many studies document that serum testosterone levels decrease
as men age. In contrast to the precipitous and profound decrease in estradiol
concentrations in women at the menopause, the decrease in testosterone levels
in men occurs moderately and gradually over a period of several decades—from
about 600 ng/dL at age 30 to about 400 at age 80. One study reported that about 20% of men over age 60 had total
serum testosterones below the normal range for young men.
A still unanswered question is whether this decrease is
physiologic (perhaps conveying a benefit) or pathologic (causing harm).
Another unanswered question is whether increasing the
low-level testosterone in elderly men to the level of younger men will exacerbate testosterone-dependent diseases such
as prostate cancer and benign prostatic hyperplasia.
Over 7 years, in a subgroup of patients without any precancerous lesions in the stomach, eradication
significantly reduced risk of developing GC.
Other investigators suggest that Hp-infected patients with
normal findings on endoscopy are at risk of development of GC. Therefore, in
high-risk populations, all patients with H
pylori infection with no precancerous lesions should consider the use of
eradication treatment for gastric cancer prevention.
Further studies are required to determine the role of
eradication in those with precancerous lesions.
A public health policy should include both the mandatory
fortification of flour and a recommendation that all women planning a pregnancy
take 5 mg a day. Each year about a
quarter of a million pregnancies result in the birth of an infant with NTD, or
an abortion performed because of such a defect. 85% of them could be prevented if all women took 5-mg daily
before pregnancy and during the first trimester.
A high percentage of women of childbearing age have
unplanned pregnancies. Since the beginning of pregnancy cannot be predicted in
these women, I believe a good case can be made to recommend all women at risk
for pregnancy routinely take FA daily. Primary care clinicians should take the
opportunity to so advise their younger women patients regardless of the reason
for the consultation.
The benefit/harm-cost ratio of FA is high. Although overall risk is low, benefit may be
great for individuals The harm is nil. Cost is low. Considering the devastating
effect of NTD for the child and the family, I believe women at risk of
pregnancy should be informed and be able to choose if the cost and
inconvenience of taking 5-mg daily FA is reasonable. RTJ
In an intermediate-to-high-risk cohort with coronary risk
factors, the risk of a non-fatal MI or CHD death in those with a FRS risk score
over 20% was 14 times that of those with a FRS of less than 10%.
The CACS significantly modified the risk prediction in all
categories of the FRS score of at least 10%,
but not when the FRS was less
than 10%. When the CRCS was more than 300, the increment in predicted risk was
equal to a 3% to 9% increase in the 10-year event risk compared with FRS alone
for every category of FRS estimate. The risk of a non-fatal MI or CHD death in
those with a CACS over 300 was 4 times that of participants with a CACS of zero.
Would adding CACS determination modify my approach to the
patient? I believe it would have no
effect. My advice about risk-factor
control would remain the same as that predicted by the FRS alone.
Primary care clinicians have a broad base of risk factors to
estimate prognosis. We do not yet adequately apply them to individual patients.
I do not believe adding another factor will be of any clinical advantage. RTJ
This is a select abstraction of an interesting article. It
describes what might be considered the obverse of the Atkins (high fat, low
carbohydrate) diet.
The HCLF diet consisted of 18% fat; 19% protein; and 63%
carbohydrate.
Subjects on the HCLF diet consumed about 600 K/cal daily less
than those in the liberal control diet.
“Low-fat, high-carbohydrate diets may reduce body
weight via reduced food intake, since complex carbohydrate-rich foods are more
satiating and less energy dense than higher-fat foods.”
Food choices in the HCLF diet were limited—no sweets
and few snacks allowed. I doubt many free-living overweight persons would
adhere to the diet for very long.
I consider this an interesting, but not a clinically
significant study. It was performed under strict observation. Food was provided by a metabolic kitchen. It
lasted only 12 weeks. There were few subjects.
Weight-loss diets have become a multimillion dollar industry.
There are many types of diet and approaches to dieting. Gullible overweight
persons in the USA seek a quick fix. There is none. None of the diets works
consistently over time. Most individuals gradually gain back any weight lost,
regardless of the diet.
A calorie is a calorie, is a calorie, is a calorie. RTJ
Strontium ranelate is an orally active agent recently re-introduced for
treatment of osteoporosis. It consists of two atoms of strontium and an organic
moiety. It acts in a dual manner to stimulate formation of new bone and
decrease bone resorption.
SR treatment
of postmenopausal osteoporosis led to early and sustained reductions in risk of
vertebral fractures. In a high-risk group of women with osteoporosis, the NNT
to prevent one new vertebral fracture over 3 years = 10
There were no significant differences between groups
in the incidence of serious adverse effects.
Diarrhea was more common in the SR group (6%). Withdrawals were similar. There
was no change in vitamin D metabolites.
“The current trial
establishes the efficacy of strontium ranelate, a familiar element relaunched
as a new compound, in reducing the risk of vertebral fractures and its role in
the armamentarium of therapy for osteoporosis.”
The increase in the red cell mass in PV causes hyperviscosity
of the blood, a major determinant of circulatory disturbance. PV is associated
with an increase in thromboxane synthesis. This suggests that
thromboxane-dependent platelet activation is a major cause of thrombosis.
Thrombotic complications are a major cause of illness and
death in untreated patients.
Long-term, low-dose aspirin, used as primary prevention,
safely prevents thrombotic complications in patients with PV. NNT to prevent
myocardial infarction, stroke, major venous thrombosis, pulmonary embolism, or
death from cardiovascular causes over 3 years = 21 to 34.
Major bleeding events associated with low-dose aspirin
occurred in one in 26.
PV is the most common of the chronic myeloprolipherative disorders.
Primary care clinicians will likely refer patients to a hematologist, but may
be responsible for long-term follow-up. RTJ
Thrombosis causes much of the illness and death in patients
with polycythemia vera. No part of the
vascular system is spared. There is a predilection for peripheral arterioles
and cerebral and abdominal vessels. Thrombosis develops in about 40% of
patients, most often before or at the time of diagnosis. Rates of fatal
thrombosis may be high. Most arterial thrombi occur in small vessels and can
cause erythromelalgia and ocular migraine. PV also is a leading cause of
hepatic vein thrombosis. Attempts to control erythrocytosis by phlebotomy often
fail to diminish the high rate of thrombosis.
Increased blood viscosity is a paramount cause of
large-vessel arterial and venous thrombosis. It is in the large vessels that
the negative effect of high hematocrit is most pronounced.
An apparently normal hematocrit may not be normal in patients with this disease.. A safe target is
under 45% in men and under 42% in women. Viscosity of the blood rises
dramatically at hematocrit levels above 45%.
The
drug maker Cephalon has made an
unusual request. It wants the FDA to approve a drug, not for a condition or a
disease, but for a symptom—sleepiness. Not just routine sleepiness, but
excessive, or “profound sleepiness”—the kind that makes drivers crash.
The drug is modafinil. It is marketed as Provigil. It is already approved for the treatment of narcolepsy.
Modafinil somehow—no one knows how—targets the hypothalamus and other
sleep-regulating areas of the brain. Patients feel more alert without
“hyperarousal”.
According to sales figures, more and more sleep experts,
psychiatrists, and primary care clinicians are prescribing modafinil for
sleepiness for conditions other than narcolepsy. Depression tops the list.
Cephalon’s trials reported few adverse effects. A handful of
patients discontinued because of headache and nausea. Modafinil induces the P450 system in the liver and may affect
metabolism of many drugs. Caution is advised in patients with left ventricular
hypertrophy, ischemic heart disease and hypertension. There is an abuse
potential. The drug has psychoactive and euphoric effects in some patients.
Modafinil is classified as a schedule IV drug. Long-term
studies are limited. The drug blurs the lines between illness and enhancement.
Provigil taken regularly costs several hundreds of dollars per
month. The company is ramping up for a marketing blitz which includes
direct-to-consumer advertising.
I do not believe primary care clinicians should
prescribe this drug. Wait for further experience. RTJ
This article is based on a collection of essays edited by
Allen Kanner and Tim Kasser--Psychology
and Consumer Culture: the Struggle for a Good Life in a Materialistic World.
“A culture of consumption, which exalts the
acquisition of material goods over almost all other values, is causing severe
psychological harm” “People who orient their lives in pursuit of the goals that
consumer society tells us to pursue are less happy.”
People who are materialistic report less satisfaction with
life, less feeling of vitality, and lower energy compared with those who prize
“intrinsic” values (personal development, family relationships, and community
involvement). They report more problems with depression, anxiety, and alcohol
and tobacco use.
Conversely, people who place a higher value on
self-knowledge, family, and friendship, are happier and have higher quality relationships,
and a greater sense of freedom.
Since the 1950s, as our economy has grown, happiness has not
changed at all. And depression and anxiety have gone up. More wealth is not
going to make us happier. It’s about
improving other aspects of our world.
I asked myself—Why did I abstract this article? What has it to do with primary care
medicine? I am not sure of the answer. Perhaps it may provide some guidance to
physicians and their families. It may enable some primary care clinicians to
provide guidance to troubled patients. RTJ
=================
1-1 TOTAL ENERGY
EXPENDITURE AND PHYSICAL ACTIVITY IN YOUNG SCOTTISH CHILDREN
The epidemic of childhood obesity has been attributed largely
to a decline in total energy expenditure (TEE). This study postulated that the lifestyle
of contemporary young children is sedentary.
In 1999 and 2000 recruited a socioeconomically representative
sample of 78 children aged 3 years. Measured TEE, mean physical activity, and
sedentary behavior. Repeated the measurements 2 years later at age 5 in 72 of
the children.
At age 3, mean physical activity level and TEE did not differ
between sexes. At age 5, mean physical activity and TEE were significantly
higher in boys:
Age
3 girls Age 3 boys Age 5 girls Age 5 boys
Time spent in sedentary behavior (%) 81 76 78 73
Both girls and boys age 3 Both
girls and boys age 5
Median time in light-intensity activity (%) 18 20
Moderate/vigorous activity (%) 2 4
Levels of TEE were low at ages 3 and 5 in both sexes,
especially in girls. Lifestyles in this sample of youngsters were sedentary.
This would increase risk of obesity. Their TEE was significantly lower than the
UK estimate average requirement for energy for children.
Children typically spent only 20-25 min per day in moderate to
vigorous physical activity. Present recommendations are that they should
accumulate at least 60 min daily. “There is a widespread perception among
parents and health and educational professionals that young children are
spontaneously active. Actually, modern children establish a sedentary lifestyle
at an early age.
Prevalence of childhood obesity has increased strikingly in
recent years.
Comment:
The authors describe sophisticated methods for measuring TEE, physical activity, and sedentary
behavior. I did not understand the techniques involved. I took their word for
them. See text for details. RTJ
========================================================================
It Is Extremely Difficult, If Not
Impossible, To Maintain A Healthy Bodyweight With A Low Level Of Physical
Activity.
1-2 PHYSICAL
ACTIVITY AND OBESITY
This editorial comments and expands on the preceding study.
The nature of human physiology is such that it is extremely
difficult, if not impossible, to maintain a healthy bodyweight with a low level
of physical activity. Technological advances have eliminated many reasons for
physical activity. Our environment encourages inactivity. It is unlikely that
we can (or want to) change the environment back to one that requires high
levels of physical activity. This means we have to teach children (and adults)
to use their intellect to push back against the environment. Such a change can
be done by eating a little less and being a little more physically active than
ordinarily. Small changes would counter the natural tendency to succumb to the
environment.
Obesity arises from an imbalance in which energy intake exceeds
energy expenditure. This means that sedentary people must maintain a low intake
of energy to avoid obesity. Human physiology did not develop to support
restriction of energy intake. It is difficult for most people to do so
consistently over time. Our environment encourages energy intake by providing
good-tasting, convenient, and inexpensive food. “Sedentary children . . . will
probably not be able to maintain energy balance and avoid obesity only by
restricting energy intake. Preventing obesity in these children will require
both reduction in energy intake and increase in physical activity. “The good news
is that it may take only small changes to prevent obesity.”
“Excessive gain in weight can be prevented by small changes in
behavior.” The average US citizen is gaining about 2 pounds a year. This gain
could occur from as little as 20-50 kcal a day ingested in excess of energy
expended. “We suggest that weight gain in 90% of the US adult population could
be prevented by reducing positive energy balance by only 100 kcal per day.”
This would equate to a little more walking (about 2000 more steps) or eating a
few less bites of food (or preferably both).
It would take a bit more to change behavior in children. The point is
that small and achievable changes in behavior can have a big impact. Walking
2000 additional steps daily and eliminating 100 kcal (eg, drinking water or a
diet drink instead of a sugared fizzy drink). Combining these two small changes
can save 200 kcal per day. Prevention of obesity is easier than treatment.
Physicians Must Be Aware Of The Costs Of
The Drugs They Prescribe.
1-3 “ME TOO” PRODUCTS—FRIEND OR FOE?
A second drug-eluting stent, another drug for erectile
dysfunction, another statin drug. Medical journals seem filled with research
articles that induce a sense of déjà vu.
Critics assert that these market latecomers often differ trivially
from earlier products and that the billions of dollars spent on marketing
me-too products could be spent in better ways. They say that these products add
little to a physician’s arsenal while driving up the costs of health care.
There is another side to the story. Me-too products create
competition among drug and device manufacturers. Competition is a powerful
driver for better quality and lower costs.
Health care leaders who struggle to provide good care with limited
resources see me-too products not as a problem, but as an important part of the
solution.
The health care “valuation equation” is sometimes summarized
as: Value = benefit *
cost.
(*
or better—benefit/harm-cost RTJ )
The equation is quite useful for understanding how drugs and
devices enter the market—or why attempts to bring them to the market may fail.
The first product in a new class defines the baseline value equation. The
manufacturer may set a high price and may have no trouble selling the product
at its asking price. When a second product in the same class comes along, its
manufacturers must offer a better value. That product must lead to a better
outcome or it must be less expensive. The current monthly costs of statins that
are expected to lower LDL-cholesterol by 45% are lower for products that
received FDA approval more recently. Costs are also lower for other recently
introduced me-too drugs.
Why don’t we see real price wars driving health costs much
lower? The biggest reason is the rapid
rate of medical progress. This causes the value to increase through steady
increases in the top half of the equation. A second or third entrant may offer
real advantages. At some point, however, technology improves and a new entrant
represents only a minimal improvement. At that point, the top part of the
equation is frozen, and the action shifts to the bottom. The manufacturer can
succeed only by competing on price. The pressure on manufacturers of 3rd
and 4th entrants to come up with a product that really improves
outcomes or lowers cost will be tremendous.
But manufacturers have learned that physicians and patients are
usually reluctant to switch from a medication that is working. So the older
drug price may remain high. And the
drug company makes larger profits by selling their drug to fewer patients at a
high price than they would with more patients paying less.
For market forces to really work, physicians have to choose
products as if costs matter.
Comment:
Primary care clinicians must be aware of the costs of the
drugs they prescribe. Current costs can be easily obtained from drug store’s
web pages. The cost of a drug containing twice the needed dose may be much less
than twice the cost. A pill cutter can
save hundreds of dollars yearly. RTJ
Nicotine
Causes An Extremely Strong Addiction Very Rapidly
1-4 WHY PEOPLE SMOKE
Cigarette smoking is primarily a manifestation of
nicotine addiction. Smokers have individual preferences for their level of
nicotine intake. They regulate the way they puff and inhale to achieve their
desired nicotine dose. “If it were not for the nicotine in tobacco, people
would be little more inclined to smoke than they are to blow bubbles.”
In addition to addiction, social, economic, personal, and
political influences all play an important part in determining patterns of
smoking prevalence and cessation. Family and wider social influences are often
critical in determining who starts smoking, who gives it up, and who continues.
Why do people start smoking?
Experimenting with smoking usually begins in the early teenage
years. It is driven predominantly by psychosocial motives. Smoking a cigarette
is a symbolic act conveying “I am no longer my mother’s child” and “I am tough”. Children who are
attracted to this adolescent assertion of perceived adulthood or rebelliousness
tend to come from backgrounds that favor smoking (eg, high levels of smoking by
parents, siblings and peers; relatively deprived neighborhoods; schools where
smoking is common). They also tend not to be succeeding according to their own
or society’s terms. They have impaired
self esteem, are overweight, or are poor achievers at school.
The desired image is sufficient for the novice smoker to
tolerate the aversion of the first few cigarettes, after which the
pharmacological factors assume much greater importance. “As the force from the
psychological symbolism subsides, the pharmacological effect takes over to
sustain the habit.”* Within a year or
so of starting to smoke, children inhale the same amount of nicotine per
cigarette as adults, experience craving for cigarettes when they cannot smoke,
make attempts to quit, and report experiencing the whole range of nicotine
withdrawal symptoms. By age 20, 80% of cigarette smokers regret that they ever
started. But, many will continue to smoke for a substantial proportion of their
lives. (*All above quotations are from Philip Morris.)
Physical and psychological
effects of nicotine:
Absorption of nicotine from the lung is almost instantaneous
and complete. With each inhalation an arterial bolus of nicotine reaches the
brain faster than by intravenous injection. (See box p 277) Nicotine has a distribution half-life of 15-20
minutes and a terminal half life of 2 hours. Smokers therefore maintain a
pattern of repetitive and transient high blood nicotine concentrations from
each cigarette. Regular hourly cigarettes are needed to maintain raised
concentrations. Overnight, blood levels fall to close to those of non-smokers.
Nicotine activates receptors which are widely distributed in
the brain. It induces the release of
dopamine. This effect is the
same as that produced by amphetamines and cocaine. Nicotine is also a
psychomotor stimulant. In new users it speeds simple reaction time and improves
performance of tasks of sustained attention. However, tolerance soon develops,
and chronic users probably do not obtain absolute improvements in performance,
cognitive processing, or mood. Smokers typically report that cigarettes calm
them down when they are stressed, and help them concentrate and work more efficiently,
but little evidence exists that nicotine provides effective self medication for
adverse mood states or for coping with stress.
A plausible explanation for why smokers perceive cigarettes to
be calming may come from a consideration of the effects of nicotine withdrawal.
Smokers start to experience impairment of mood and performance within hours of
their last cigarette, and certainly overnight. These effects are completely
alleviated by smoking a cigarette. Smokers go through this process thousands of
times over the course of their smoking career. This may lead them to identify
cigarettes as effective self relief rather than any absolute improvement.
Symptoms of nicotine
withdrawal:
Much of the intractability of cigarette smoking is thought to
stem from withdrawal symptoms—irritability, restlessness, feeling miserable,
impaired concentration, and increased appetite—as well as craving for
cigarettes. These symptoms begin within hours and are maximal during the first
week. Most then resolve over 3 to 4 weeks, but hunger can persist for months.
Cravings, sometimes intense, can persist for months. Nicotine replacement
reliably attenuates the severity of withdrawal.
An intimate coupling of behavior rituals and sensory aspects of
smoking with nicotine uptake gives ample opportunity for secondary
conditioning. Each puff is linked to the sight of the packet, the smell of the
smoke, and the scratch of the throat some 70 000 times each year. Smokers are
concerned that if they quit they would not know what to do with their hands.
Other factors encourage smoking: being married to a smoker; being part of a social network in a
socially disadvantaged group among whom the prevalence of smoking is so high as
to constitute a norm.
The natural course of cigarette smoking is typically the onset
of regular smoking in adolescence, followed by repeated attempts to quit. Each
year about a third of adult smokers try to quit, usually unaided, and typically
relapsing within days. In general, less
than 3% of attempts to quit result in sustained cessation.
Regulation of nicotine intake:
Smokers show a strong tendency to regulate their nicotine
intakes within narrow limits. They avoid intakes that are too low (withdrawal
symptoms), or too high (nicotine overdose). Within individuals, nicotine
preferences emerge early and seem to be stable over time. The phenomenon of
nicotine titration is responsible for the failure of intakes to decline after
switching to cigarettes with low tar and nicotine. Compensatory puffing and
inhalation, operating at a subconscious level, ensure that nicotine intakes are
maintained. As nicotine and tar delivery in smoke are closely related,
compensatory smoking likewise maintains tar intake. This defeats any potential
health gain from low tar cigarettes.1
Socioeconomic
status and nicotine addiction.
An emerging phenomenon of the utmost significance is the
increasing association of continued smoking with markers of social disadvantage.
Affluent persons are much more likely to quit. Smokers who are poor tend to
have higher levels of nicotine intake and are substantially more dependent. It
is evident that future progress in reducing smoking is increasingly going to
have to tackle the problems posed by poverty.
Smoking as a chronic disease:
Cigarette dependence is a chronic relapsing condition that for
many users extends over decades. Successful interventions need to tackle the
interacting constellations of factors—personal, family, socioeconomic, and
pharmacological—that sustain use and can act as major barriers to cessation.
1 Some have
wondered why the nicotine content of cigarettes is not artificially increased
in the manufacturing process. This would supply the needed nicotine and
automatically lower the intake of carcinogens. Nicotine itself is not
carcinogenic.
I presume this would lead to all sorts of ethical and legal
complications.
The first article in this
clinical review The Problem of Tobacco
Smoking by Richard Edwards,
University of Manchester, UK (BMJ January
24, 2004; 328 : 217-219) comments:
Cigarette smoking is one of the biggest avoidable causes of
death and disability and one of the biggest threats of current and future world
health. “For most smokers, quitting smoking is the single most important thing
they can do to improve their health. Encouraging smoking cessation is one of
the most effective and cost effective things that doctors and other health
professionals can do to improve health and prolong their patient’s lives.
Cessation has substantial and immediate long-term health
benefits for smokers of all ages. The excess risk of death from smoking falls
soon after cessation and continues to do so for at least 15 years. Former
smokers live longer than continuing smokers, no matter what age they stop.
Smokers who stop before age 35 have about the same length of life as non-smokers.
Stopping before age 30 removes 90% of the lifelong risk of lung cancer. The
risk of heart disease decreases quickly after cessation. Within a year, risk is
halved. Within 15 years, the risk is almost the same as never-smokers.
Stopping before or in the first 3 to 4 months of pregnancy
protects the fetus against the reduced birth weight associated with smoking.
Preoperative cessation reduces perioperative mortality and complications.
“Early cessation is especially important.”
1-5 OMEGA 3
FATTY ACIDS AND CARDIOVASCULAR DISEASE—Fishing For A Natural Treatment
Omega 3 fatty acids (O3FA) from fish and fish oils can protect against coronary heart
disease (CHD). In this era of
polypharmacy, many persons believe that simple dietary interventions or
nutritional supplements may be a more natural and acceptable method of
providing benefits.
The optimum intake of O3FA is not established. Their method of
action is not understood. Some studies report no association, particularly in
populations with already moderate fish consumption. Concerns about
environmental contamination of fish have been raised.
These investigators performed a literature search and reviewed
the evidence regarding associations between O3FA and CHD.
Epidemiological and
observational studies:
Over 30 years ago, it was established that Greenland Inuits had
a low mortality from CHD despite a diet rich in fat (especially O3FA in fish,
seal, and whale). Fatty fish (mackerel, herring, salmon, sardines and trout)
are a rich source of O3FA and O6FA. Two to three servings a week should provide
about 1 g/d of O3FA.
Most studies have shown an inverse association between fish
consumption and CHD. A high concentration of O3FA reduces rate of sudden death.
A systemic review of 11 prospective cohort studies concluded that fish intake
reduced mortality due to CHD in populations at increased risk.
The Diet and Reinfarction Trial (DART) randomized over 200 men
with a recent myocardial infarction. Men who received advice on fish had a 29%
reduction in mortality over 2 years, mainly due to a reduction in death from
CHD. An Italian study reported a relative risk reduction of 30% in
cardiovascular death, and a 45% reduction in sudden death over 3.5 years. Benefits were apparent within 4 months.
Mechanism of action:
Several possible mechanisms have been proposed. None is
established. The predominant effect may be antiarrhythmic. O3FA are readily
incorporated into atherosclerotic plaques. This may make plaques less
vulnerable to rupture. O3FA also have a direct effect on endothelial function.
A modest reduction in BP has been reported.
O3FA reduce triglycerides in a dose-dependent manner. The reduction may
reach 30%. Effects on cholesterol are small.
Clinical implications:
O3FA from fish or fish oil supplements should be considered for
secondary prevention of patients
after MI. Diet should include at least 2 servings of oily fish weekly. Fish oil
capsules should be considered for those unable to tolerate fish or are unable
to change their diet effectively. “Approved pharmaceutical grade capsules
should be prescribed . . .”
The bottom line:
The American Heart Association recommends:
Patients without
documented CHD should eat a variety of fish (preferably oily) at least twice
weekly. Diet should also include vegetable oils.
Patients with
documented CHD should consume 1 g of O3FA and O6FA daily, preferably from oily
fish.
Physicians may prescribe 2-4 g/d of O3FA daily,
provided as capsules, for patients with hypertriglyceridemia.
Terminology of polyunsaturated fatty acids:
Number of carbon atoms (eg, C18) Number of double bonds (eg, 6) Position of first double bond from CH3 end
(eg, n-3; omega 3)
Omega 3 fatty acids Food
source
Plant derived:
Linolenic acid C18: 3 n-3 Flaxseed, soybean, walnut, and
rapeseed (canola) oil
Marine derived:
Eicosapentanoic acid C20: 5 n-3 Fish;
shellfish
Docosahexanoic acid C22:
6 n-3
Omega 6 fatty acids:
Plant derived: Linoleic
acid C18 4 n-6 Corn,
safflower, and sunflower oils.
Derived from linoleic acid ;
Arachidonic acid C20 4 n-6
Docosapentanoic acid
C22 5 n-6
Omega
3 FA and omega 6 FA are essential polyunsaturated fatty acids. O6FA are
abundant in the Western diet in the form of vegetable oils rich in linoleic
acid. Omega 9 fatty acids are in olive oil, peanuts, avocados, and almonds.
Comment:
Omega 3 and Omega 6 are included in the healthy Mediterranean
diet which has been reported convincingly to reduce risk of CHD. Persons with and without CHD should consume more fish.
There was a flurry of
interest in over-the-counter fish oil capsules about 10 years ago. My
pharmacist says that there is still some demand, but it has decreased.
The article presents several websites and reviews. RTJ
1-6 MEMANTINE
TREATMENT IN PATIENTS WITH MODERATE TO SEVERE ALZHEIMER DISEASE ALREADY
RECEIVING DONEPEZIL
The FDA has limited treatment for Alzheimer disease (AD) to monotherapy with
anti-cholinesterase inhibitors. In October 2003, the FDA approved memantine for
treatment of moderate to severe AD. Memantine is a blocker of the receptor for
aspartate. It is a new class of drug.
An open-label study suggested that a combination of memantine
with various anti-cholinesterase drugs was well tolerated. This study
hypothesized that adding memantine (Namenda)
to donepezil (Aricept ) would result
in clinical benefit and would be well tolerated.
Conclusion: Memantine resulted in significant
statistical, but only slight clinical benefit when added to donepezil. It
appeared safe.
STUDY
1. Randomized, controlled trial compared memantine vs
placebo in over 400 patients (mean age = 75)
All had moderate to severe AD. (Mini-mental State Examination scores 5
to 14. Mean = 10) All were already receiving stable doses of
donepezil. (Mean = 10 mg.)
2. Randomized to:
1) Memantine (titrated up to 20 mg dally) + continued donepezil, or 2)
Placebo + continued donepezil.
3. Outcome measures included: Measure of change in cognition and
activities of daily living, and clinician’s + caregiver’s impression of change.
1. Changes from baseline over
24 weeks:
Baseline 24 weeks
Placebo Memantine Placebo Memantine
SIB 1 80 78 -2.4 +
1.0
ADL 2 35.8 35.5 -3.3 -1.7
CIBIC-Plus 3 4.66 4.41 4.64 4.38
NPI 4 13.4 13.4 +
2.9 - 0.5
BGP Care dependency subscale 5 9.8 9.5 + 2.2 +
0.6
2 ADL
(activities of daily living) is a 19-item inventory focusing on activities of
daily living in later stages of dementia. Possible scores range from 0 to
54—higher scores reflect higher functioning. (Note that this measure declined in the memantine group, but not
as great as in the placebo group.
3 CIBC-Plus
(clinicians interview-based impression of change plus caregiver input) assesses
the clinician’s impression of effect of medication on overall clinical status, and incorporates caregiver
observations on a scale from 1 (marked improvement) to 7 (a marked worsening).
(Note that the change in CIBC-Plus in the memantine group was from 4.41
to 4.38 – hardly a clinical benefit. They do state that the P value = 0.03
4 NPI (neuropsychiatric inventory) assesses
frequency and severity of behavioral symptoms based on an interview with the
caregiver. Score ranges from 0 to 144. Higher scores reflect greater symptoms.
5 BGP
(behavioral scale for geriatric patients) assesses observable aspects of
cognition, function, and behavior. (A higher score reflects worse function.)
(The investigators
stressed that all differences in outcomes were statistically significant. But,
are they clinically significant? They
state—“No clinically significant differences were detected between treatment
groups in the mean change to end point.” Note the difference in the CIBIC-Plus
was slight—from 4.41 to 4.38 in the memantine group. (P value = 0.03.)
Although statistically significant, hardly of clinical significance.)
1. “Efficacy of memantine was significantly better than placebo treatment for treatment of moderate to severe AD in community-dwelling patients. Specifically, measures of cognitive function, activities of daily living behavior, and clinical global status were significantly improved with memantine compared with placebo.”
2. No pharmacokinetic or pharmacodynamic interactions were observed between donepezil and memantine. They act in different ways. Memantine has an effect on the glutamate-aspartate receptor system; donepezil affects cholinesterase
3. The long-term benefits were not addressed by this
study.
Comment:
Sponsored by Forrest
Laboratories. My pharmacy quotes $155
for a month’s supply of memantine (20 mg daily). An interesting
sidelight—memantine is a relative of the old drug used for influenza—amatadine.
Memantine has also been reported to lead to benefit in
patients with vascular dementia and mixed dementia.
There is evidence that the excitatory effect of glutamate
plays a role in the pathogenesis of AD. Memantine is a low-affinity blocker of
aspartate receptors. This may prevent excitatory amino acid neurotoxicity
without interfering with the physiological actions of glutamate for memory and
learning.
Investigators, as in this report, often stress
statistically significant improvement, not clinical improvement. This may be
misleading. In my view, the outcome of this study is disappointing. The
investigators place a spin on benefits by noting the statistically significant
outcomes. This may appear to be an impressive result, but it is not clinically
important.
It may be that families will encourage this approach, hoping
that their loved one may be an outlier, and receive more benefit.
I would be interested in a study comparing effects of these
drugs in patients with mild or possibly beginning AD — those with frequent
occurrence of “senior moments”
(temporary forgetfulness of names of well-known friends and past events which
they recalled immediately when they were younger). RTJ
As “Baby
Boomers” Age, Many Will Request Replacement Therapy
1-7 RISKS OF
TESTOSTERONE-REPLACEMENT THERAPY AND RECOMMENDATIONS FOR MONITORING.
Review articles are too long
to abstract concisely. I enjoy reading them and sometimes abstract a few points
which are new to me, which I had forgotten, or which I consider important and
deserving emphasis
Hypogonadism is a clinical condition in which low levels of
serum testosterone are found in association with specific signs and
symptoms: diminished libido and sense
of vitality, erectile dysfunction, reduced muscle mass and bone density,
depression, and anemia.
It is estimated to affect up to 4 million men in the USA.
Prevalence increases with age. Few men receive replacement therapy. About 50% of
men over age 80 and 30% of men age 70-79 have low serum levels. (Defined as a total serum testosterone under
325 ng/dL. Are these “low” levels physiologic or pathologic? I vote for
physiologic. RTJ)
Reports indicate that testosterone replacement may produce a
wide range of benefits: improvement in
libido, bone density, muscle mass, body composition, mood, erythropoiesis, and
cognition.
Recent interest has been fueled by medical awareness of the
effects of hypogonadism, media attention regarding hormone replacement,
marketing of new topical testosterone formulations, and the desire of “baby
boomers” to maintain vigor and health into their more mature years.
Controversy remains regarding indications for testosterone
supplementation in aging men. The most controversial topic is the issue of
risk. No studies have yet been initiated to assess benefits and risks,
especially possible stimulation of prostate cancer. Despite the controversy,
prescriptions for testosterone supplementation have increased substantially
over the past decade.
This review discusses what is known and not known about
regarding risks and to provide recommendations for monitoring men who receive
it.
Injectable, transdermal, buccal, and oral formulations are
available in the USA. Injectable preparations are typically given at a dose of
100 mg once a week. This produces high
peak levels and a “roller coaster” effects on symptoms.
A transdermal-patch preparation is available to deliver 5 to 10
mg. It requires daily application. Relatively uniform blood levels are
achieved. Levels above the physiologic range should be discouraged. (Note this is replacement to the level of
younger men, not above. RTJ)
Oral preparations are discouraged because of adverse effects on
the liver.
The author discusses many possible risks especially on benign
prostatic hyperplasia (BPH) and
prostate cancer (PC).
BPH: Multiple studies
have failed to demonstrate exacerbations of voiding symptoms and residual urine
volumes in men receiving replacement therapy.
Urinary retention has not occurred at serum levels higher than controls.
But, prostate volume does increase significantly during replacement to a level
equal to that of men without hypogonadism.
PC: If lowering
testosterone levels causes PC to regress, does elevating levels cause PC to
appear? Case reports have suggested conversion of an occult PC into a
clinically apparent PC. To date, prospective studies have demonstrated a low
frequency of association between replacement therapy in hypogonadal men and PC.
There has been no follow-up beyond 36 months. It is of some concern that the
underlying prevalence of PC in men with low testosterone levels appears to be
substantial even in those with a normal PSA and digital rectal examinations.
“Despite decades of research, there is no compelling evidence
that testosterone has a causative role in prostate cancer”. There is no compelling evidence to suggest
that men with higher testosterone levels are at greater risk of PC or that
treating men with hypogonadism with exogenous androgens increases risk.
“In our opinion, proper monitoring with measurement of PSA and
digital rectal examination should promote the early diagnosis and thus
potential cure of most ‘unmasked’ prostate
cancers identified during testosterone treatment.” Certainly all men who
present for possible testosterone replacement who are found to have abnormal
PSA should undergo biopsy. A rapid rise in PSA or development of an abnormal
digital rectal examination during therapy should also indicate biopsy. (The
authors advocate routine biopsy in all men presenting for replacement therapy.)
“There is no need to withhold testosterone treatment once a
negative biopsy result has been obtained.”
Comment:
I asked myself if I wasted my time in abstracting these
articles. Should primary care clinicians deal with this problem? Should they
refer patients seeking therapy to a urologist with considerable
experience? At the present stage of
development, I would follow the second course.
The value of a therapy has been described as: Value =
benefits
harms-costs
I believe the benefits are somewhat nebulous and unknown
long-term. Harms are potentially great. Cost is considerable considering
consultation and laboratory fees as well as the cost of the testosterone. My pharmacy quotes a monthly cost of $168
for patches delivering 5 mg daily.
========================================================================
Wait Until
More Evidence is Available
1-8
HYPOGONADISM IN ELDERLY MEN—WHAT TO DO UNTIL THE EVIDENCE COMES
This editorial comments and expands on the preceding article
A long-awaited report from the Institute of Medicine (IOM)
concluded that there is insufficient evidence that testosterone benefits
elderly men.
Many studies document that serum testosterone levels decrease
as men age. In contrast to the precipitous and profound decrease in estradiol
concentrations in women at the menopause, the decrease in testosterone levels
in men occurs moderately and gradually over a period of several decades. (From
about 600 ng/dL at age 30 to about 400 at age 80.) One study reported that about 20% of men over age 60 had total
serum testosterones below the normal range for young men.
A still unanswered question is whether this decrease is
physiologic (perhaps conveying a benefit) or pathologic (causing harm).
In men a reductase converts testosterone to the active
androgen, dihydrotestosterone; in women an aromatase converts it to estradiol.
Testosterone also acts directly on androgen receptors to affect muscle, bone
marrow, bone, and brain. Testosterone has many effects on many tissues
One reason for thinking that the decrease might be pathologic
in older men is the parallel between the consequences of frank hypogonadism
caused by pituitary and testicular disease and the consequences of aging: decrease in bone density, muscle mass and strength,
energy, and libido. In truly pathologic states, administration of testosterone
corrects these deficiencies.
Studies in elderly men with low-normal levels have generally
shown an increase in lean body mass, a decrease in fat mass, and a trend toward
an increase in bone density, but no clear improvement in muscle strength or
libido.
Another unanswered question is whether reversing the low-level
testosterone in elderly men will exacerbate testosterone-dependent diseases
such as prostate cancer, benign prostatic hyperplasia, erythrocytosis, and
perhaps sleep apnea. No data answers this question.
For elderly men with low-normal testosterone levels, the IOM has concluded that efficacy has not been demonstrated sufficiently well to justify a long-term study to determine risks of testosterone replacement. The committee recommended, as a first step, short-term randomized, placebo-controlled studies.
Meanwhile, practicing physicians remain in a quandary. There
are a few basic principles for guidance:
The criteria for diagnosis of deficiency should be more stringent in the absence, than in the presence of a disease that is known to cause hypogonadism (eg, pituitary macroadenoma).
Criteria for diagnosis should be more stringent in
elderly men. It should be considered if
the early morning serum total testosterone is consistently and
unequivocally subnormal. (eg, below 200 ng/dL)
When the testosterone level is unequivocally low, the
serum leuteinizing concentration should be measured. An elevated level indicates
primary (testicular) hypogonadism. A non-elevated level indicates secondary
(pituitary) hypogonadism.
Until efficacy and safety of testosterone treatment is
established, the prudent course is to limit it to those who are more severely
hypogonadal.
Men who are treated should be monitored by serum
testosterone levels to ensure relative stability. (Oral therapy should not be
used, it is associated with liver dysfunction.) Recipients should also be monitored for possible exacerbation of
testosterone-dependent diseases (eg, prostate cancer and hyperplasia).
The response of presenting symptoms is much harder to
interpret because symptoms are non-specific.
These
principles constitute a “wait until the evidence comes” approach.
These recommendations call for a complicated, detailed, and
expensive initial investigation and an
equally complicated follow-up. I
doubt many primary care clinicians would be willing to offer replacement
therapy on this basis. RTJ
====================================================================
Helicobacter
pylori Has Been Categorized As A Group I Carcinogen.
1-9
HELICOBACTER PYLORI ERADICATION TO PREVENT GASTRIC CANCER IN A HIGH-RISK
REGION OF CHINA
“The association between chronic Helicobacter pylori (Hp)
infection and development of gastric cancer (GC) is well established.”
It has been categorized as a group I carcinogen.
Before the development of adenocarcinoma, the infected gastric
mucosa progresses through stages:
chronic active gastritis; glandular atrophy; and intestinal metaplasia and dysplasia. All of
these changes are precancerous.
This study asked: What is the effect of Hp eradication on prevention of gastric cancer?
Conclusion; Only in the
subgroup of subjects without
precancerous lesions did eradication significantly decrease development of GC.
1. Population-based, randomized, placebo-controlled primary prevention trial followed 1630
healthy carriers of Hp (mean age = 42) from a high-prevalence area of
China. All were endoscoped and biopsied. Of the 1630 patients, 988 (61%) did not
have any precancerous lesion.
2. Randomized to:
1) Hp eradication therapy, or 2) Placebo Eradication therapy consisted
of a 2-week course of omeprazole (20 mg), a combination amoxicillin/clavulanate
(750 mg), and metronidazole (400 mg)—all twice daily.
3. Outcome measures: Primary = incidence of GC;
Secondary = incidence of GC in patients with and without precancerous lesions.
4. Follow-up = mean of 7.5 years.
1. Overall, 18 new cases of GC developed (7 treated;
11 placebo). No significant difference
between groups.
2. In the subgroup without
any precancerous lesions on presentation, none of the treated patients
developed GC vs 6 of the placebo treated patients. (P = 0.02)
3. Smoking (hazard ratio = 6.2) and older age (hazard
ratio 1.1 per year increment) were independent risk factors for GC.
1. Overall, in this primary prevention trial, there
was no difference in incidence of GC between groups.
2. In the subset without
any precancerous lesion there was a significant difference. No patient in the
treated group developed GC vs 6 in the placebo group. (P = 0.02)
3. Other studies have reported that Hp eradication can
prevent development of a second GC after endoscopic mucosal resection of early
GC.
4. It is still uncertain whether Hp eradication can
reverse early precancerous lesions in the stomach. Is there a point of
no-return? The investigators believe there is a stage at which changes are not
reversible.
5. Other investigators suggest that Hp-infected
patients with normal findings on endoscopy are at risk of development of GC.
Therefore, in high-risk populations, all patients with H pylori infection with no precancerous lesions should consider
eradication treatment for gastric cancer prevention.
Over 7 years, in a subgroup of patients without any precancerous lesions in the stomach, eradication
significantly reduced risk of
developing GC,
Further studies are required to determine the role of
eradication in those with precancerous lesions.
Comment:
The authors state that there may be a point of no-return. Ie,
once a precancerous lesion has developed, eradication will not reduce risk of
gastric cancer.
If I were infected, I would be treated. RTJ
Almost All
Neural Tube Defects Can Be Prevented
1-10 FOLIC
ACID AND THE PREVENTION OF NEURAL TUBE DEFECTS
Folic acid (FA)
supplementation before pregnancy and during its early stages markedly reduces
the risk of neural-tube defects (NTD).
NTD may be considered to represent a vitamin-deficiency disorder. All women who
are planning to become pregnant should take folic acid supplements beginning
before pregnancy and continuing through its early stages. Once a pregnancy has
been confirmed, it is probably too late.
A study in this issue of NEJM (January 8, 2004; 350: 134-42) reported that women who had a
pregnancy complicated by NTD had antibodies to folate receptors. This suggests
a pathogenesis, and how supplementation may prevent NTD.
What should guide public health policy? At what dose will FA
prevent nearly all NTD?
A given dose of FA adds a constant increment to the plasma
folate level, irrespective of dietary folate intake. A given percentage
increase in the plasma level results in a constant percentage reduction in the
risk of NTD. In the background of a
serum folate level of 5 ng per mL, which is typical in many Western countries,
a dose of about 5 mg per day is expected to decrease the risk of NTD by
85%. Little is gained by higher doses.
A dose of 0.4 mg (the amount in a standard multivitamin) reduces risk by an
estimated 36%. The average level of food fortification in the USA of about 0.2
mg per day reduces risk of NTD by about 20%. The food fortification level is
unnecessarily low. Achieving sufficient
levels through dietary change is impractical.
There is no evidence that FA fortification masks B12 deficiency.
A public health policy should include both the mandatory
fortification of flour and a recommendation that all women planning a pregnancy
take 5 mg a day. Each year about a
quarter of a million pregnancies result in the birth of an infant with NTD, or
an abortion performed because of such a defect. 85% of them could be prevented if all women took 5-mg daily
before pregnancy and during the first trimester.
Comment:
A high percentage of women of childbearing age have unplanned
pregnancies. Since the beginning of pregnancy cannot be determined in these
women, I believe a good case can be made to recommend all women at risk for
pregnancy routinely take 5 mg FA daily. Primary care clinicians should take the
opportunity to so advise their younger women patients regardless of the reason
for the consultation.
5-mg folic acid is available only by prescription at a cost
of about 10 cents per tablet ~ $3 a month. Alternatively, over-the-counter six
800 micrograms tablets cost about the same.
The benefit/harm-cost ratio of FA is high. Although overall risk is low, benefit may be
great for individuals The harm is nil. Cost is low. Considering that NTD are
devastating for the child and the family, I believe women should be informed
and choose if the cost and inconvenience of taking 5-mg daily FA is reasonable.
RTJ
Is Adding This Expensive Test Clinically Significant?
1-11 CORONARY
ARTERY CALCIUM SCORE COMBINED WITH FRAMINGHAM SCORE FOR RISK PREDICTION IN
ASYMPTOMATIC INDIVIDUALS.
Guidelines advise that all adults undergo coronary
heart disease (CHD) risk assessment
to guide preventive treatment.
The Framingham Risk Score (FRS)1 is
a statistical model that uses age, smoking history, blood pressure,
cholesterol, HDL-cholesterol, blood glucose levels, and history of diabetes to estimate coronary event risk.
There is a continuing search for additional tests to improve
prediction.
This study assessed the coronary artery calcium score (CACS) as an additional test to improve
prediction.
Conclusion: High CACS,
combined with the FRS, can improve risk predictions.
1. Entered over 1450 asymptomatic patients (mean age =
65, mostly male) in 1990-92. The great
majority had at least one abnormal coronary risk factor which placed them at
over 10% estimated 8-year risk of
developing coronary heart disease (CHD)
according to the FRS.
2. None had previous history of CHD or diabetes.
3. At year 3, 1312 surviving participants underwent a
second evaluation including a computerized tomography scan (CT) to determine presence and extent of coronary calcification.
4. Followed yearly for a median of 7 years after the
CT scan. Subjects developing diabetes were excluded, leaving 1029 to complete
the study. These subjects were divided into 4 groups according to their coronary artery calcium score. (CACS range 0
to over 300.)
5. Main outcome measure = non-fatal myocardial
infarction (MI) or CHD death.
1. The risk of a non-fatal MI or CHD death in those
with a CACS over 300 was 4 times that of participants with a CACS of zero.
2. The risk of
a non-fatal MI or CHD death in those with a FRS risk score over 20% was 14
times that of those with a FRS of less than 10%.
3. Events Framingham
Risk Score
0-9 10-15 16-20 Over
20
E/P* HR* E/P* HR* E/P* HR* E/P*
HR*
CACS risk score
0 0/46 1.0 2/79 1.0 5/116 3.4 7/75 7.2
1-100 0/19 1.0 4/97 3.2 8/126 5.3 9/79 9.0
101-300 0/14 1.0 3/40 6.2 5/64 6.2 7/53 12.5
> 300 1/19 4.6 8/41 17.6 8/77 8.9 17/84 19.1
(*E/P = events/patients * HR = hazard ratio)
1. Over a median of 7 years, in asymptomatic patients
without diabetes and at least one risk factor for CHD but no prior clinical
CHD, the FRS alone was able to rank participants according to CHD event risk in
a graded fashion
2. CACS alone was also able to rank CHD event risk
independently of the FRS.
3. The CACS significantly modified the risk prediction in all categories of the FRS score of at least 10%, but not when the FRS was less than 10%. When the CRCS was more than 300, the increment in predicted risk was equal to a 3% to 9% increase in the 10-year event risk compared with FRS alone for every category of FRS estimate.
4. The receiver operating characteristic curves, however
showed little advantage of FRS + CACS over FRS alone (0.68 vs 0.63).
5. Among the patients with CACS of zero, the absence
of CASC did not preclude risk of a CHD event.
In this intermediate to high risk cohort with coronary risk
factors measured by FRS, a CACS of more than 300 was associated with a
significant increase in CHD event risk compared with that determined by FRS
alone.
A CACS of zero did not markedly lower risk as predicted by the
FRS.
1 Go to: www.nhlbi.nih.gov/guidelines/cholesterol/atglance/pdf for the Adult Treatment III Quick Desk
Reference. It contains a copy of the FRS which you can use to determine
individual risk.
Comment:
I abstracted this article in detail because some clinicians
may become very enthusiastic about adding this expensive risk assessor. The
question primary care clinicians must ask is:
Would adding CACS determination modify my approach to the patient? I believe it would have no effect. My advice about risk-factor control would
remain the same as that predicted by the FRS alone.
Primary care clinicians have a broad base of risk factors to
estimate prognosis. We do not yet adequately apply them to individual patients.
I do not believe adding another factor will be of any practical advantage. RTJ
1-12 EFFECTS OF
AN AD LIBITUM LOW-FAT, HIGH-CARBOHYDRATE DIET ON BODY WEIGHT, BODY
COMPOSITION, AND FAT DISTRIBUTION IN OLDER MEN AND WOMEN.
This is a select abstraction of an interesting article. It
describes what might be considered the obverse of the Atkins (high fat, low
carbohydrate) diet.
The study was based on prior evidence suggesting that
high-carbohydrate, low-fat (HCLF)
diets reduce total energy intake and increase satisfaction.
Conclusion: An ad lib
HFLC diet with no attempt at energy intake resulted in weight loss.
1. Entered and randomized 24 volunteers age 55 to 80
(mean = 65). All were overweight (mean BMI= 31; weight stable) and sedentary.
None were smokers. Some had impaired glucose tolerance. All completed the
study.
2. Randomized to a 12-week : 1) HCLF diet, 2) Control diet.
1) HCLF
diet consisted of 18% fat; 19% protein; and 63% carbohydrate.
2) Control
diet consisted of 41% fat, 14% protein, and 45% carbohydrate.
3. Diets were prepared 3 times daily in a metabolic kitchen and designed to provide 150% of predicted energy requirement. Subjects were instructed to eat as much or as little as they wished.
4. Participants were informed that the purpose of the
study was to determine the effects of a heart healthy diet on general disease
risk. Thus, there was little overt motivation to lose weight.
1. Outcomes over 12 weeks Control diet HCLF diet
Energy intake (kcal/d) 2825 2250 *
Protein (% of energy) 15% 19%
Fat (% of energy) 41% 18%
Carbohydrate (% of energy) 45% 63%
Body weight loss -0.1
kg -3.2 kg
(* Note the difference in energy intake
between groups both of which were instructed to eat as much as they desired.
Why the difference? I suspect it was
due in part to the monotony of the HCLF
diet. RTJ.)
2. No change between groups in
resting metabolic rate or fat oxidation.
1. Ad-lib consumption of this
HCLF diet over 12 weeks resulted in significant loss of body weight
2. The HCLF diet was not an
eat-any-carbohydrate you wish. It consisted mainly of complex carbohydrates.
Breakfast Cereal
Lunch and dinner Vegetarian chili, lentils,
carrots, boiled potato, rice, beans, spaghetti with tomato sauce
Some meat: sliced
ham, baked chicken breast, hamburger patty, baked fish, tuna.
Breads Blueberry
muffin, whealtbagel, English muffin, whole wheat bread, cornbread
Sweets and snacks Lemon
pudding, crispbread crackers, popcorn
Fruit Variety
Vegetables Variety
Beverages Apple
juice, cranberry juice, orange juice,
Dairy products Skim
milk, non-fat yogurt, shredded cheddar cheese,
3. Despite being fed to maintain body weight, individuals
complained that they were given too much food. They were never hungry.
4. “Low-fat, high-carbohydrate diets may reduce body
weight via reduced food intake, since complex carbohydrate-rich foods are more
satiating and less energy dense than higher-fat foods.”
Comment:
Dr. William J Evans, one of the investigators, kindly
e-mailed me a list of foods provided.
Food choices in the HCLF diet were limited—no sweets and few
desserts allowed. I doubt many free-living overweight persons would adhere to
the diet for very long.
I consider this an interesting, but not a clinically
significant study. It was performed under strict observation. Food was provided
by a metabolic kitchen. It lasted only 12 weeks. There were few subjects.
Weight-loss diets have become a multimillion dollar industry.
There are many types of diet and approaches to dieting. Overweight persons in
the USA seek a quick fix. There is none. None of the diets consistently works
over time. Most individuals gradually gain back any weight lost, regardless of
the diet.
A calorie is a calorie, is a calorie, is a calorie. RTJ
Vertebral deformities in women with osteoporosis
predict further vertebral fractures.
The bone fragility characterizing osteoporosis after the
menopause results from an imbalance in bone remodeling causing bone resorption
to exceed bone formation. Antiresorptive therapies reduce the rate of
remodeling and lower fracture rate. The increase in bone mineral density
observed in clinical trials of these drugs is the result of more complete
secondary mineralization of the existing (but reduced) bone tissue mass. Restoration of bone tissue mass and bone
structure is not achieved with antiresorptive drugs. This requires use of
anabolic agents.
Strontium ranelate 1 (SR) is an orally active agent now proposed for treatment
of osteoporosis. It consists of two atoms of strontium and an organic moiety.
It acts in a dual manner to stimulate formation of new bone and decrease bone
resorption .
To date, no deleterious effects on mineralization of bone have
been reported.
This study assessed the efficacy of SR against vertebral
fractures in postmenopausal women with osteoporosis. And its safety.
Conclusion: Treatment
led to early and sustained reductions in risk of vertebral fractures.
1. A phase 3 trial randomized to over 1600 postmenopausal women (mean age 69; mean 21 years since menopause). All had osteoporosis (mean T score = -3.5) and a history of at least one minimal-trauma vertebral fracture. All received a run-in period of 2 to 24 weeks of calcium and vitamin D, depending on severity of deficiency.
2. Randomized to:
1) 2 g of oral SR daily, or 2) placebo
3. All received supplementary calcium and vitamin D.
4. X-rayed vertebra and measured bone mineral density
(BMD) periodically. BMD at the lumbar
spine was measure by dual-energy x-ray absorptiometry and adjusted for
strontium content.2
5. Follow-up = 3 years.
1. About 1400 women made up
the population of the intention-to-treat analysis.
2. Outcomes at 3 years: Strontium Placebo NNT*
New vertebral fractures 18% 28% 10
More than one new vertebral fracture 6.4% 9.8% 29
Symptomatic vertebral fractures 11.3% 17.4% 16
Reported back pain 17.7% 21.3% 28
(* Number of patients needed to treat for 3 years to prevent
one fracture or back pain.)
2. Over 3 years fewer patients in the strontium group
lost at least 1 cm in height.
3. No difference in non-vertebral fractures.
4. Adjusted for strontium content2, bone
mineral density at the lumbar spine increased over base-line in the strontium
group by 6.8% vs a decrease of 1.3% in the placebo group
5. The strontium group had an increase in the serum
bone-specific alkaline phosphatase (increased bone formation) and a lower
concentration of C-telopeptide (decreased resorption) compared with placebo.
6. Adverse effects: There were no significant differences between groups in the
incidence of serious adverse effects. Diarrhea was more common in the SR group
(6%). Withdrawals were similar. There was no change in vitamin D metabolites.
1. SR decreased risk of new vertebral fractures at one
year and at 3 years.
2. The reduction was similar to that reported from
alendronate and risedronate. And
slightly lower than the reduction with parathyroid hormone, a bone-forming drug.
3. The authors suggest, on the basis of blood levels
of biochemical markers, that SR acts by a combination of increasing bone
formation and decreasing bone resorption.
SR treatment of postmenopausal osteoporosis led to early and
sustained reductions in risk of vertebral fractures.
1 Strontium was
originally detected in lead mines near Strontian, Scotland in the late 1700s.
2 Any metal with
an atomic number greater than calcium can influence BMD. The atomic number of
strontium
is 38; calcium, 20. My brief search failed to find the
formula for ranelic acid.
Comment:
There was a flurry of interest in fluoride several years ago.
Enthusiasm decreased because bone became more fragile. There was no indication
of this association with SR in this study. I spent the considerable time to
abstract this study because of its potential importance as an effective, safe
and likely inexpensive therapeutic agent. Primary care clinicians be on the
lookout for developments RTJ
An editorial in this issue of NEJM (pp 504-06) by Ghada
El-Hajj Fuleihan, American University of Beirut Medical Center, Lebanon.
comments and expands:
Strontium is present in trace amounts in food and water, and
throughout the skeleton. Areas of active osteogenesis take up a large percent
of strontium.
Strontium was used years ago for osteoporosis. It fell out of
favor because mineralization defects were detected and synthesis of calcitriol
was inhibited. These adverse effects were thought possibly due to
calcium-deficient diets and the doses used. In the past decade interest has
been renewed.
In contrast to other
therapies for osteoporosis, strontium appears to induce uncoupling of bone
remodeling, simultaneously stimulating bone formation and reducing bone
resorption.
“The current trial establishes the efficacy of
strontium ranelate, a familiar element relaunched as a new compound, in
reducing the risk of vertebral fractures and its role in the armamentarium of
therapy for osteoporosis.”
Low-Dose
Aspirin Effectively Prevents Major Thrombotic Complications
1-14 EFFICACY
AND SAFETY OF LOW-DOSE ASPIRIN IN POLYCYTHEMIA VERA
The increase in the red cell mass in polycythemia vera
(PV) causes hyperviscosity of the
blood, a major determinant of circulatory disturbance. Thrombotic complications
are a major cause of
illness and death in untreated
patients. Chemotherapy and phlebotomy
are used in patients at high risk of thrombotic events.
PV is associated with an increase in thromboxane synthesis.
This suggests that thromboxane-dependent platelet activation is a major cause
of thrombosis.
This study assessed the effect of low-dose aspirin on risk of
thrombotic complications in patients with PV.
Conclusion: Low-dose
aspirin prevented thrombotic complications.
1. A randomized, double-blind, placebo-controlled
trial enrolled over 500 patients (mean age 60) with PV to assess the efficacy
and safety of low-dose aspirin. None had conditions which called for
antithrombotic therapy.
2. At baseline: mean hematocrit = 49; red-cell count =
5900; white-cell count = 10,500; platelet count = 380 000.
3. Over 50% had been treated with phlebotomy and/or
chemotherapy.
4. Randomized to:
1) 100 mg enteric-coated aspirin daily, or 2) placebo
5. End-points:
A) Cumulative rate of non-fatal myocardial infarction (MI) , non-fatal stroke, or death from
cardiovascular causes; B) Cumulative
rate of non-fatal MI, non-fatal stroke, pulmonary embolism, major venous thrombosis, or death from cardiovascular causes.
6. Follow-up at intervals up to 60 months. (Mean = 3
years.)
1. Compared with placebo, aspirin was associated with
a reduced risk of end-point A (relative risk = 0.41), and a reduced risk of
end-point B. (RR= 0.40).
2. Overall mortality and
cardiovascular mortality were not reduced significantly.
3. Incidence of major bleeding
episodes were increased in the aspirin group.
4. Endpoints: Aspirin (%) Placebo (%) Absolute difference (%)
NNT
Primary A 2 4.9 2.9 34
Primary B 3.2 7.9 4.7 21
5. Major bleeding 9.1 5.3 3.8 26 (harm)*
(* P value = 0.08; relative risk = 1.6, CI = (0.27 to 9.71)
DISCUSSION
1. The rationale for this trial was based on 3
considerations:
1)
Synthesis of platelet thromboxane is increased in PV.
2) Low-dose
aspirin effectively suppresses platelet thromboxane
3) A
previous trial found low-dose aspirin well-tolerated.
2. Most patients enrolled in this trial had no
previous thrombotic events. The trial can be considered a primary prevention trial.
3. The benefit of aspirin was detectable after about
180 days.
4. Patients with PV have an increase in the synthesis
of thromboxane by a factor of approximately 10. This can be largely suppressed
by low-dose aspirin. The authors believe the increased production of thromboxane
is the primary target of aspirin.
5. An important finding was the moderate increase in
the risk of bleeding. (RR= 1.6) This is consistent with previous observations.
Nevertheless, the authors recommend the use of aspirin to prevent thrombotic complications
in patients with PV.
Long-term, low-dose aspirin safely prevented thrombotic
complications in patients with PV.
Comment:
Low-dose aspirin should be routinely advised for
patients with PV who have no contraindication. The benefit/harm-cost ratio is
high.
Aspirin, even in low-dose is associated with an increased
risk of bleeding. (Note the skewed confidence interval—0.27 to 9.71.) Once a
major bleed has occurred, further aspirin is contraindicated.
PV is the most common of the chronic myeloprolipherative
disorders. Primary care clinicians will likely refer patients to a
hematologist, but may be responsible for long-term follow-up. RTJ
========================================================================
1-15 DAILY
ASPIRIN—ONLY HALF THE ANSWER
This editorial comments and expands on the preceding
study.
The long-term consequences of the unregulated hematopoiesis in
patients with polycythemia vera include:
extramedullary production of blood (liver and spleen), painful and debilitating
organomegaly, portal hypertension, hyperuricemia and secondary gout, renal
stones, pruritus, hemorrhage (usually mucocutaneous), and thrombosis.
Myelofibrosis, bone marrow failure, and acute leukemia may ensue. Chemotherapy
with alkylating agents is associated with malignant transformation.
Thrombosis causes much of the illness and death. No part of the
vascular system is spared. There is a predilection for peripheral arterioles
and cerebral and abdominal vessels. Thrombosis develops in about 40% of
patients, most often before or at the time of diagnosis. Rates of fatal
thrombosis may be high. Most arterial thrombi occur in small vessels and can
cause erythromelalgia and ocular migraine. PV also is a leading cause of
hepatic vein thrombosis. Attempts to control erythrocytosis by phlebotomy often
fail to diminish the high rate of thrombosis.
PV is unique among conditions causing erythrocytosis. The
increase in red cell mass is accompanied not
by a reduction in plasma volume, but often by an expansion. It is not possible
to estimate the red-cell mass on the basis of the hematocrit. An apparently
normal hematocrit may not be normal
in patients with this disease.. A safe target is under 45% in men and under 42%
in women. Viscosity of the blood rises dramatically at hematocrit levels above
45%.
Platelet activation and utilization in PV are increased.
Neutrophils and endothelial cells are also activated. Release of the von
Willebrand factor provides the final component for inappropriate initiation of
coagulation.
The microvascular syndromes (erythromelalgia and ocular
migraine) are independent of blood viscosity. They arise from widespread
platelet and endothelial activation, facilitated by the high shear rate in
arterioles. Platelet aggregates form on endothelial cells. Aspirin arrests this
process.
Increased blood viscosity is a paramount cause of large-vessel
arterial and venous thrombosis. It is in the large vessels that the negative
effect of high hematocrit is most pronounced. But endothelial cell activation
is also important.
Comment:
What is the normal range of hematocrit? Authorities do not agree. Normal range
according to:
Female (%) Male (%)
SI units 33-43 39-49
NEJM 37-48 42-52
Dictionary 37-47 42-52
1-16 POISED TO
CHALLENGE NEED FOR SLEEP, “WAKEFULNESS ENHANCER” ROUSES CONCERN
The drug maker Cephalon
has made an unusual request. It wants the FDA to approve a drug, not for a
condition or a disease, but for a symptom--sleepiness. Not just routine
sleepiness, but excessive, or “profound sleepiness”--the kind that makes
drivers crash.
The drug is modafinil. It is marketed as Provigil. It is approved for the treatment of narcolepsy. Now,
about 90% of prescriptions are going for off-label uses. A Washington Post article recently recommended it for jet-lag. A New Yorker author found it helpful for
late-night writing marathons. A world champion sprinter took it before a race.
A TV commentator commented that when taking it “I feel quite awake. I don’t
feel the heart racing thing that caffeine sometimes does. A bit jumpy, a bit
extra something going on here”.
The FDA’s central nervous system advisory committee was less
than enthusiastic about Cephalon’s request. It did give the go-ahead to include
indications for two new diagnoses--obstructive sleep apnea, and shift-work sleep
disorder. It did not endorse use in patients with other causes of sleepiness.
There was concern that patients may view it as a replacement for the normal
amount of nighttime sleep. “We would never advocate that there is a substitute
for sleep.” The FDA rebuked Cephalon
for running advertisements that provided the “overwhelming misleading
impression that Provigil can be used
to improve wakefulness in all patients presenting with symptoms of daytime
sleepiness. But according to sales
figures, more and more sleep experts, psychiatrists, and primary care
clinicians are prescribing modafinil for sleepiness not caused by narcolepsy.
Depression tops the list.
What about adverse effects?
“It’s the drugs safety record that is winning over clinicians.” Cephalon’s trials reported few adverse
effects. A handful of patients discontinued because of headache and nausea. A
jittery feeling was less frequent than in patients taking methylphenidate (Ritalin). Amphetamines work by revving up the entire body, increasing BP
and heart rate. Modafinil somehow—no one knows how—targets the hypothalamus and
other sleep-regulating areas of the brain. Patients feel more alert without
“hyperarousal”. Modafinil is classified as a schedule IV drug. It has some
abuse potential. Long-term studies are limited. The drug blurs the lines
between illness and enhancement.
The drug is cleared from the blood quickly enough so that shift
workers can sleep when they are ready. Outside the laboratory, sleep
specialists say that they have repeatedly seen modafinil rejuvenate miserable
patients. But all the sleep experts interviewed expressed concern that patients
and physicians will confuse modafinil’s symptom relief with a treatment for the
underlying condition. Chronic short sleepers are at higher risk for
cardiovascular problems, hypertension, heart failure and stroke. They have a
higher overall mortality rate.
Provigil costs
several hundreds of dollars per month. The company is ramping up for a
marketing blitz which includes direct-to-consumer advertising.
Comment:
I felt that the article overall would lead to greater use
rather than discouraging it.
My PDR gives additional information:
The blood concentration reaches a steady state in 2
to 4 days. The half life is 15 hours. I wonder--how does this jive with the
statement in the text that the drug is cleared fast enough so that shift
workers can sleep when they are ready?
Modafinil induces the P450 system in the liver and may affect
metabolism of many drugs.
Caution is advised in patients with left ventricular
hypertrophy, ischemic heart disease and hypertension.
There is an abuse potential. The drug has psychoactive and
euphoric effects in some patients.
I do not believe primary care clinicians should prescribe
this drug. Wait for further experience.
RTJ
Earn As Much
As You Can; Save As Much As You Can; Give As Much As You Can.
1-17 SHOPPING
‘TIL WE DROP: Can Psychology Save Us From Our Lust For Possessions?
(This article is based on a
collection of essays edited by Allen Kanner and Tim Kasser--Psychology and Consumer Culture: the
Struggle for a Good Life in a Materialistic World)
“A culture of consumption, which exalts the
acquisition of material goods over almost all other values, is causing severe
psychological harm. Yet it is ignored
by the psychology profession.”
Consumption is one of the most important psychological issues
of our times, but it is getting scant attention. The profession prefers to deal
with problems at the level of individuals, families, and small groups, not
culture. There is a social taboo against criticizing capitalism in the USA.
This prevents psychologists from objectively looking at the harm that is being
done by the current economic and social system. The profession of psychology has been deeply involved in the
creation of the consumer culture of today—in particular by helping to create
modern marketing techniques.
To make the case that consumerism is worthy of psychology’s
attention, the editors have been applying the methods used to study disorders
such as depression and anxiety to assess the relation between the importance
that people place on material values and their sense of happiness and
well-being. “The basic finding is that people who orient their lives in pursuit
of the goals that consumer society tells us to pursue are less happy.”
To be happy, people need to feel safe and secure. They need to
feel competent and able to do the things they need to do. They need to feel connected to people and
loved. They need to feel free and autonomous.
These values are not often advertised much in society, except as
a way to sell something.
Most research shows that people who place a high value on
attaining financial success, having nice possessions, and having the right
image and high status based on wealth and possessions score lower on several
measures of well-being. People who are
materialistic report less happiness, less satisfaction with life, less feeling
of vitality, and lower energy compared with those who prize “intrinsic” values
(personal development, family relationships, and community involvement). They
report more problems with depression, anxiety, and alcohol and tobacco use.
Conversely, people who place a higher value on self-knowledge,
family, and friendship, are happier and have higher quality relationships, and
a greater sense of freedom.
Some psychologists disagree. They say that the desire for more
material things is associated with poor mental health only when it is
associated with certain motives—the desire for power or “lording it over”
others; a desire to show off, prove yourself, and to show that you are not as
stupid as everyone says you are. These motives are all rooted in self-doubt.
There are many healthy motives for acquiring wealth—to attain financial
security; provide for your family, and your children’s education; to enjoy a
comfortable life; and to buy goods you personally enjoy. “It is not the desire
for goods as such that is bad for people, but it’s desiring them for the wrong
reasons.”
Some people are more vulnerable to materialistic appeals than
others—in particular people who come from poorer backgrounds, from broken
homes, and from families in which the parents are cold and controlling. These
people are insecure. If you want to feel secure, buy this, become rich, latch
on to materialistic values as a way to feel good about yourself
Material things may help you feel good (or less bad) for a
little while, but they don’t do anything to solve the underlying problem.
Since the 1950s, as our economy has grown, happiness has not
changed at all. And depression and anxiety have gone up. More wealth is not
going to make us happier. It’s about
improving other aspects of our world.
Comment:
I asked myself—Why did I abstract this article? What has it to do with primary care
medicine? I am not sure of the answer. Perhaps it may provide some guidance to
physicians and their families. It may enable some primary care clinicians to
provide guidance to troubled patients.
I believe many people, young and old, are adopting a more
caring, less materialistic lifestyle. They are opting for spending more time
with family and in community service. And placing less value on owning the
biggest house, and the most expensive automobiles.
Some time ago I read a short 3-item suggestion for pursuing a
good lifestyle: 1) Earn all you can
2) Save all you can 3) Give all you can. ( I wish I could remember where I read it. RTJ )
Earning requires you to obtain the best education and
training possible, and then to apply it honestly in the workplace. The goal is
to secure a safe, comfortable home; to educate your children; and to provide
for your continuing independence in old age.
Saving means not living ostentatiously—living “below your
means”; not being profligate, but conserving.
Giving is the hardest—at least giving wisely. There are
multitudes of causes which will make good use of your gifts and time for the
general welfare. I believe you should give
as much as you can to your children in time of need, and a legacy large enough
to help then get them started on the same path you have trod—but not enough to
deter them from earning their own way through life. RTJ
=============
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Best wishes,
Richard James Editor/publisher