How Early Should Obesity Prevention Start?

Obesity has pervaded the United States and is spreading throughout the world. Following in its wake is type 2 diabetes, which will affect at least half a billion people worldwide by 2030. A majority of U.S. women of childbearing age are overweight or obese (as defined by a body-mass index [BMI, the weight in kilograms divided by the square of the height in meters] >25). These women are likely to gain excessive weight when they’re pregnant, making it harder for them to return to their prepregnancy weight after delivery. Postpartum weight retention not only portends increased lifelong risks for obesity-related complications but also an increased BMI at the inception of future pregnancies. During pregnancy, excessive weight gain, along with other risk factors such as gestational diabetes, can alter fetal growth and metabolism, leading to higher adiposity in the offspring. If the child is female, grows up obese, and becomes pregnant, the cycle begins again. It is time to interrupt this vicious cycle to prevent obesity and chronic diseases in mothers and children.

Once obesity is present, it is challenging to treat because of multiple physiological, behavioral, and cultural feedback loops. The good news is that the prenatal period and the first postnatal year hold critical clues that may lead to interventions to reduce obesity in women and prevent it in children. In a range of animal models (from rodents to nonhuman primates), dietary, hormonal, mechanical, and other perturbations that occur prenatally and during infancy induce lifelong, often irreversible derangements in the offspring’s adiposity and metabolism. These changes involve the environmental alteration of genetic expression, in part through epigenetic mechanisms, rather than changes in the genome itself. Thus, timely intervention during the early, plastic phases of development — unlike corrective efforts made later in life — may lead to improved lifelong health trajectories.

Because of challenges in measuring fetal exposures and the long latency between initial determinants and salient health outcomes, however, it is difficult to translate such proofs of principle in animals to human populations. The first generation of developmental-origins studies in humans linked birth weight to adult obesity-related morbidity and mortality. We now recognize that birth weight and each of its components, gestational duration and fetal growth, are low-resolution, momentary markers for myriad prenatal and perinatal influences. In the past decade, many such influences have been identified and quantified in epidemiologic studies that have involved the period before birth, used modern methods to mitigate confounding, and incorporated biomarkers. These studies have identified prenatal risk factors for obesity ranging from lifestyle factors such as the mother’s smoking status to psychosocial factors including antepartum depression, medical conditions such as gestational diabetes, physiological stress as reflected by fetal exposure to glucocorticoids, and epigenetic markers such as gene-specific DNA methylation levels in umbilical-cord tissue.

After birth, rapid weight gain in the first 3 to 6 months of life is a potent predictor of later obesity and cardiometabolic risk. Lactation cannot be the entire explanation, because breast-fed babies tend to gain more weight than formula-fed babies in the first few months of life. The perinatal hormonal milieu may very well be a contributing factor. In one study, higher leptin levels in umbilical-cord blood, chiefly reflecting placental production, were associated with slower gain in infant weight-for-length and lower adiposity at the ages of 3 years and 7 years. In contrast, higher leptin levels at 3 years of age were associated with faster gains in BMI from 3 to 7 years, suggesting that leptin resistance develops between birth and 3 years of age.1 These findings are consistent with studies in animals showing a critical period of perinatal leptin exposure that allows normal maturation of appetite-regulating neurons in the hypothalamus. Features of infant feeding other than breast versus bottle may also play a role. Among formula-fed infants, the introduction of solids before 4 months was associated with a sixfold increase in the odds of obesity 3 years later.2

Emerging risk factors for obesity include exposure to endocrine disruptors, which appear to do the most damage during times of maximum developmental plasticity, and the gut microbiota. Our bodies contain about 1013 cells but as many as 1014 microorganisms. Certain modifications in the number and type of microorganisms during infancy are associated with excess weight gain, at least in rodents. The infant gut is normally colonized during transit through the birth canal, which could be one reason why children delivered by cesarean section appear to be at elevated risk for obesity.3

Given obesity’s numerous developmental determinants, it is logical that effective prevention would target multiple modifiable factors. In combination, two well-studied prenatal risk factors, excessive gestational weight gain and maternal smoking during pregnancy, and two postnatal factors, fewer months of breast-feeding and a shorter duration of daily sleep during infancy, are associated with wide variation in childhood obesity. In one study, preschool-age children whose mothers did not smoke or gain excessive weight during pregnancy and who were breast-fed for at least 12 months and slept for at least 12 hours per day during infancy had a predicted obesity prevalence of 6%, as compared with 29% among children for whom the opposite was true for all four risk factors4; the rates were similar (4% and 28%, respectively) when the children reached 7 to 10 years of age (see graphPredicted Probability of Obesity at 7 to 10 Years of Age for 16 Combinations of Four Modifiable Prenatal and Postnatal Risk Factors.). These observational data raise the possibility that avoiding some or all of these risk factors could substantially reduce the proportion of childhood obesity.

Preventing racial and ethnic disparities in obesity risk will also require a developmental approach. By school age, rates of obesity among black and Hispanic children in the United States are higher than the rates among white children, even after adjustment for socioeconomic circumstances. Many of the risk factors during pregnancy and early childhood are more prevalent among nonwhite persons, and they explain a substantial proportion of racial and ethnic differences in obesity in mid-childhood.5

Several features of pregnancy and infancy make the prenatal and postnatal periods conducive to behavior change to reduce the risk of obesity and its complications. First, women appear especially willing to modify their behavior during these periods to benefit their children. Second, since pregnant women and infants receive frequent routine medical care, interventions involving improved health care delivery have great potential. Third, these periods are relatively brief, and we know that behavior-change interventions are typically most successful in the short term. Fourth, if effective interventions begun during pregnancy are maintained after birth, they will reduce the risk of maternal obesity for future pregnancies and thus help to interrupt the intergenerational cycle.

Ongoing intervention studies promise to inform medical practice and public health. Many current trials target excessive gestational weight gain, including seven randomized, controlled trials funded by the National Institutes of Health that will together include more than 1000 overweight or obese women and follow infants through at least 1 year of age. It remains to be proven, however, that reducing gestational weight gain reduces the obesity risk in offspring. An alternative approach focuses on dietary quality, independent of calorie content, to ameliorate maternal insulin resistance and excessive placental nutrient transfer. Pilot studies have suggested that a multiple-risk-factor approach during infancy, targeting mothers as conduits for changes in their infants, can improve sleep duration and delay the introduction of solid foods.

But even as we await the results of obesity-prevention trials, some recommendations are warranted because of their beneficial effects on other health outcomes. Pregnant women should not smoke. Treatment of gestational diabetes reduces macrosomia at birth, although such treatment hasn’t been proven to prevent obesity. U.S. rates of elective cesarean sections have apparently leveled off, but reducing these rates, especially of cesarean sections performed before 39 weeks of gestation, is a public health goal. Simple sleep-hygiene measures are worth trying, even in early infancy. The ideal age, in terms of allergy prevention, for introducing solid foods appears to be 4 to 6 months, and further research may show that the same is true in terms of obesity prevention.


Source: NEJM

C difficile: Obesity Linked to Community-Onset Infections.

Obesity may be a risk factor for Clostridium difficile infection (CDI), according to results from a retrospective cohort study of 132 cases seen at a tertiary care medical center.

After potential confounders were taken into account, patients with simple community-onset infections were more than 4 times as likely to be obese as patients who had community-onset infections that came shortly after an exposure to a healthcare facility, according to data reported in an article published in the November issue ofEmerging Infectious Diseases.

“Obesity may be associated with CDI, independent of antibacterial drug or health care exposures,” write the researchers, led by Jason Leung, MD, from the University of Michigan Hospital in Ann Arbor. Such an association could help explain the uptick of community-onset cases in individuals having low levels of traditional risk factors.

The authors propose that obesity may perturb the intestinal microbiome in ways similar to those seen with inflammatory bowel disease and use of antibiotics, both of which are known risk factors for CDI.

“Translational research could help elaborate the dimensions of the interaction of the intestinal microbiota with C. difficile in obese patients,” the researchers maintain. They also suggest that an investigation of a dose–response relationship between body mass index and infection risk might be informative.

“[I]t is critical to establish whether obesity is a risk factor for high rates of C. difficile colonization, as is [inflammatory bowel disease]; if that risk factor is established, prospective observations would improve understanding of whether obesity plays a role in the acquisition of CDI, or alters severity of disease and risk for recurrence,” they write.

As for the patients with community-onset infections after healthcare exposure, the study’s findings highlight “the importance of increased infection control at ancillary health care facilities and surveillance for targeting high-risk patients who were recently hospitalized.”

In the study, the researchers reviewed the microbiology results and medical records of all patients who had laboratory-proven, nonrecurrent CDI at Boston Medical Center in Massachusetts during a 6-month period.

When the patients were classified according to the setting of disease onset, 43% had infections that began in the community without recent exposure to a healthcare facility, 30% had infections that began in a healthcare facility, and 23% had infections that began in the community within 30 days of exposure to a healthcare facility (most often a hospital or long-term care facility).

The prevalence of obesity, defined as a body mass index exceeding 30 kg/m2, was 34% in the group with community-onset infections compared with 23% in the general population (odds ratio, 1.7; 95% confidence interval [CI], 1.02 – 2.99). The value stood at 13% in the group with community-onset healthcare-associated infections and 32% in the group with healthcare-onset infections.

In multivariate analyses, patients with simple community-onset infections were significantly less likely to be older than 65 years (odds ratio, 0.35; 95% CI, 0.13 – 0.92; P < .05) and more likely to be obese (odds ratio, 4.06; 95% CI, 1.15 – 14.36; P < .05) than patients with community-onset healthcare-associated infections.

In addition, patients with simple community-onset infections were significantly less likely to have prior antibiotic exposure (odds ratio, 0.29; 95% CI, 0.11 – 0.76; P < .05) than patients with healthcare-onset infections. There was also a trend whereby they were much more likely to have inflammatory bowel disease (odds ratio, 6.40; 95% CI, 0.73 – 56.17; P < .10).

Finally, patients with community-onset healthcare-associated infections were dramatically less likely to have had prior antibiotic exposure than patients with healthcare-onset infections (odds ratio, 0.08; 95% CI, 0.02 – 0.28; P < .05).

Mid-life stress ‘precedes dementia’

stressed woman
Mid-life stress may increase a woman’s risk of developing dementia, according to researchers.

In a study of 800 Swedish women, those who had to cope with events such as divorce or bereavement were more likely to get Alzheimer’s decades later.

The more stressful events there were, the higher the dementia risk became, BMJ Open reports.

The study authors say stress hormones may be to blame, triggering harmful alterations in the brain.

Stress hormones can cause a number of changes in the body and affect things such as blood pressure and blood sugar control.

“Start Quote

Current evidence suggest the best ways to reduce the risk of dementia are to eat a balanced diet, take regular exercise, not smoke, and keep blood pressure and cholesterol in check”

Dr Simon Ridley Alzheimer’s Research UK

And they can remain at high levels many years after experiencing a traumatic event, Dr Lena Johansson and colleagues explain.

But they say more work is needed to confirm their findings and ascertain whether the same stress and dementia link might also occur in men.

Stress link

In the study, the women underwent a battery of tests and examinations when they were in either their late 30s, mid-40s or 50s, and then again at regular intervals over the next four decades.

At the start of the study, one in four women said they had experienced at least one stressful event, such as widowhood or unemployment.

A similar proportion had experienced at least two stressful events, while one in five had experienced at least three. The remaining women had either experienced more than this or none.

During follow-up, 425 of the women died and 153 developed dementia.

When the researchers looked back at the women’s history of mid-life stress, they found the link between stress and dementia risk.

Dr Johansson says future studies should look at whether stress management and behavioural therapy might help offset dementia.

Dr Simon Ridley, of Alzheimer’s Research UK, said that from this study, it was hard to know whether stress contributed directly to the development of dementia, whether it was purely an indicator of another underlying risk factor in this population of women, or whether the link was due to an entirely different factor.

“We know that the risk factors for dementia are complex and our age, genetics and environment may all play a role. Current evidence suggests the best ways to reduce the risk of dementia are to eat a balanced diet, take regular exercise, not smoke, and keep blood pressure and cholesterol in check.

“If you are feeling stressed or concerned about your health in general, we would recommend you talk this through with your GP.”

Hydration before contrast cuts CIN in high-risk patients.

Even patients with advanced kidney disease can steer clear of contrast-induced nephropathy (CIN) if given plenty of hydration, say researchers from the Netherlands. Results from the study of nearly 1,000 patients with stage 3 or 4 kidney disease were published in the June issue of Radiology.

The study found that fewer than 2.5% of the patients examined developed CIN when current guidelines emphasizing hydration were followed, according to the researchers from Radboud University Nijmegen Medical Centre in the Netherlands. The study also found that heart failure, low body mass index, and repeat contrast administration were associated with CIN.

CIN is the third most common cause of acute renal failure in hospitalized patients, and while most cases are limited to mild and transient impairment of renal function, serious morbidity and mortality, as well as longer hospital stays, can occur.

“In current practice, hydration is considered the preventive method of choice; however, evidence supporting its use is limited,” wrote Dr. Corinne Balemans and colleagues. Previous studies have relied on a variety of hydration protocols that were often used inconsistently (Radiology, June 2012, Vol. 263:3 pp. 706-713).

Balemans and colleagues aimed to determine risk factors associated with CIN by evaluating its incidence in patients with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m2 who received iodinated contrast media intravenously and were treated using current guidelines.

Current CIN guidelines developed in Europe and the U.S. emphasize the identification of patients at high risk for CIN and the use of hydration as a preventive measure, either using normal saline or sodium bicarbonate as an alternative option, they wrote.

In the study, patients with renal insufficiency were evaluated at a special outpatient clinic where CIN was assessed and normal saline hydration was prescribed (Centraal Begeleidings Orgaan guidelines, 2007), with renal function assessed after the procedures.

The researchers stratified all patients with eGFR less than 60 mL/min/1.73 m2 for risk of CIN; those at high risk based on absolute GFR and risk factors were hydrated with 1,000 mL of isotonic saline before and after contrast injection. Serum creatinine was measured three to five days later, and CIN was defined as an increase of 25% or more from baseline. Finally, the authors recorded and compared risk factors between patients with CIN and those without using stepwise multiple logistic regression analysis.

The study included 747 patients (43% female; mean age, 71.3 years ± 10) who underwent 944 procedures. Patients were hydrated in 511 (54.1%) procedures. CIN developed after 23 procedures (2.4%).

Independent predictors of CIN were heart failure (odds ratio, 3.0), body mass index (BMI) (odds ratio, 0.9), and repeated contrast material administration (odds ratio, 2.8), Balemans and colleagues wrote. No patients needed dialysis.

The population was carefully prepared before iodinated contrast injection, and only 7.7% of patients at high risk for CIN did not receive hydration.

“Our study provides reliable estimates of CIN and shows that the incidence of CIN is low in a homogeneous population of patients with stage 3 or 4 chronic kidney disease who underwent treatment in accordance with existing guidelines and who received intravenous iodinated contrast material,” the authors wrote.

In the study, money was saved by restricting hydration to about half of the study population; patients at high risk for CIN were hydrated, whereas those at low risk were not. However, it’s possible the incidence could have been reduced further by a less restrictive policy.

Regarding heart failure, a well-known risk factor for CIN, such patients may have more severe atherosclerotic vascular disease and are more prone to hemodynamic changes during and after procedures. For them, hydration may not be helpful, the authors wrote.

The inverse association between BMI and CIN may not have been reported previously, they noted. Patients with low BMI usually have a lower percentage of muscle mass, and as a result the formulas used to calculate eGFR overestimate renal function, Balemans and colleagues wrote.

Another study reported the association between repeat contrast exposure and CIN. In that study (Trivedi and Foley), the increased risk was even notable in patients with preserved renal function.

As for study limitations, the population was large but the number of events was small. Absolute GFR was used to classify risk, and there is debate about whether GFR should be corrected for body surface area.

The incidence of CIN in patients with stage 3 or 4 chronic kidney disease is low when treated in accordance with current guidelines, the authors concluded.

“Our findings support the efficacy of hydration regimens,” they wrote. “The risk of CIN is increased in patients with heart failure, low BMI, and repeated contrast material administration. These risk factors need to be validated in future studies.”

Populations at risk for severe or complicated influenza illness: systematic review and meta-analysis.


Objective To evaluate risk factors for severe outcomes in patients with seasonal and pandemic influenza.

Design Systematic review.

Study selection Observational studies reporting on risk factor-outcome combinations of interest in participants with influenza. Outcomes included death, ventilator support, admission to hospital, admission to an intensive care unit, pneumonia, and composite outcomes.

Data sources Medline, Embase, CINAHL, Global Health, and the Cochrane Central Register of Controlled Trials to March 2011.

Risk of bias assessment Newcastle-Ottawa scale to assess the risk of bias. GRADE framework to evaluate the quality of evidence.

Results 63 537 articles were identified of which 234 with a total of 610 782 participants met the inclusion criteria. The evidence supporting risk factors for severe outcomes of influenza ranged from being limited to absent. This was particularly relevant for the relative lack of data for non-2009 H1N1 pandemics and for seasonal influenza studies. Limitations in the published literature included lack of power and lack of adjustment for confounders was widespread: adjusted risk estimates were provided for only 5% of risk factor-outcome comparisons in 39 of 260 (15%) studies. The level of evidence was low for “any risk factor” (odds ratio for mortality 2.77, 95% confidence interval 1.90 to 4.05 for pandemic influenza and 2.04, 1.74 to 2.39 for seasonal influenza), obesity (2.74, 1.56 to 4.80 and 30.1, 1.74 to 2.39), cardiovascular diseases (2.92, 1.76 to 4.86 and 1.97, 1.06 to 3.67), and neuromuscular disease (2.68, 1.91 to 3.75 and 3.21, 1.84 to 5.58). The level of evidence was very low for all other risk factors. Some well accepted risk factors such as pregnancy and belonging to an ethnic minority group could not be identified as risk factors. In contrast, women who were less than four weeks post partum had a significantly increased risk of death from pandemic influenza (4.43, 1.24 to 15.81).

Conclusion The level of evidence to support risk factors for influenza related complications is low and some well accepted risk factors, including pregnancy and ethnicity, could not be confirmed as risks. Rigorous and adequately powered studies are needed.

What is already known on this topic

  • Certain patient populations are thought to be at higher risk for developing complicated or severe influenza illness
  • These groups are prioritised for vaccination as well as for antiviral treatment
  • The quantity and quality of evidence on risk factors for developing complicated or severe influenza illness is limited
  • While some risk factors could be corroborated, evidence to support other, well established risk factors for severe outcomes could not be found

What this study adds

Source: BMJ

Why Take Follow-Up Biopsies in Celiac Disease?

Results provide status of mucosal healing, which is associated with risk for lymphoma.
Celiac disease is a risk factor for T-cell lymphomas of the intestine as well as a variety of other malignancies. Some experts believe that adherence to a gluten-free diet mitigates this risk. Guidelines suggest repeating serologic testing after several months on a gluten-free diet, but follow-up biopsy sampling to confirm healing is not routinely performed. Now, researchers consider its value for assessing cancer risk.

To examine the association between mucosal healing in celiac disease and the risk for lymphoproliferative malignancy (LPM), investigators in Sweden conducted a retrospective, population-based cohort study of 7625 patients with celiac disease who had at least one follow-up biopsy taken after diagnosis. Biopsies were taken at least 6 months after initiation of a gluten-free diet and at a median of 1.3 years after diagnosis. LPM occurrence was determined using a nationwide cancer registry.

In multivariate analysis, patients with persistent villous atrophy on follow-up biopsy had a higher risk for LPM compared with the general population (standardized incidence ratio, 3.78; 95% confidence interval, 2.71–5.12) and compared with patients with mucosal healing (hazard ratio, 2.26; 95% CI, 1.18–4.34). The risk estimate was highest for T-cell lymphoma, though not statistically significant. Total or subtotal villous atrophy was more strongly associated with T-cell lymphoma (HR, 9.23) than partial or no villous atrophy (HR, 3.4).


This study confirms the increased risk for lymphoproliferative malignancy in patients with celiac disease. Further, it documents for the first time that the risk for LPM, particularly T-cell lymphoma, is predicted by the degree of mucosal healing on follow-up biopsy. These findings strongly suggest that, as in inflammatory bowel disease, mucosal healing is an important therapeutic goal. Follow-up biopsy at 6 to 12 months after initiation of a gluten-free diet should be considered, with the goal of achieving resolution of villous atrophy.

Source: NEJM

Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis.


Lower extremity peripheral artery disease is the third leading cause of atherosclerotic cardiovascular morbidity, following coronary artery disease and stroke. This study provides the first comparison of the prevalence of peripheral artery disease between high-income countries (HIC) and low-income or middle-income countries (LMIC), establishes the primary risk factors for peripheral artery disease in these settings, and estimates the number of people living with peripheral artery disease regionally and globally.


We did a systematic review of the literature on the prevalence of peripheral artery disease in which we searched for community-based studies since 1997 that defined peripheral artery disease as an ankle brachial index (ABI) lower than or equal to 0·90. We used epidemiological modelling to define age-specific and sex-specific prevalence rates in HIC and in LMIC and combined them with UN population numbers for 2000 and 2010 to estimate the global prevalence of peripheral artery disease. Within a subset of studies, we did meta-analyses of odds ratios (ORs) associated with 15 putative risk factors for peripheral artery disease to estimate their effect size in HIC and LMIC. We then used the risk factors to predict peripheral artery disease numbers in eight WHO regions (three HIC and five LMIC).


34 studies satisfied the inclusion criteria, 22 from HIC and 12 from LMIC, including 112 027 participants, of which 9347 had peripheral artery disease. Sex-specific prevalence rates increased with age and were broadly similar in HIC and LMIC and in men and women. The prevalence in HIC at age 45—49 years was 5·28% (95% CI 3·38—8·17%) in women and 5·41% (3·41—8·49%) in men, and at age 85—89 years, it was 18·38% (11·16—28·76%) in women and 18·83% (12·03—28·25%) in men. Prevalence in men was lower in LMIC than in HIC (2·89% [2·04—4·07%] at 45—49 years and 14·94% [9·58—22·56%] at 85—89 years). In LMIC, rates were higher in women than in men, especially at younger ages (6·31% [4·86—8·15%] of women aged 45—49 years). Smoking was an important risk factor in both HIC and LMIC, with meta-OR for current smoking of 2·72 (95% CI 2·39—3·09) in HIC and 1·42 (1·25—1·62) in LMIC, followed by diabetes (1·88 [1·66—2·14] vs 1·47 [1·29—1·68]), hypertension (1·55 [1·42—1·71] vs 1·36 [1·24—1·50]), and hypercholesterolaemia (1·19 [1·07—1·33] vs 1·14 [1·03—1·25]). Globally, 202 million people were living with peripheral artery disease in 2010, 69·7% of them in LMIC, including 54·8 million in southeast Asia and 45·9 million in the western Pacific Region. During the preceding decade the number of individuals with peripheral artery disease increased by 28·7% in LMIC and 13·1% in HIC.


In the 21st century, peripheral artery disease has become a global problem. Governments, non-governmental organisations, and the private sector in LMIC need to address the social and economic consequences, and assess the best strategies for optimum treatment and prevention of this disease.

Source: Lancet.


Adult Stature and Risk of Cancer at Different Anatomic Sites in a Cohort of Postmenopausal Women.


Background: Prospective studies in Western and Asian populations suggest that height is a risk factor for various cancers. However, few studies have explored potential confounding or effect modification of the association by other factors.

Methods: We examined the association between height measured at enrollment in 144,701 women participating in the Women’s Health Initiative and risk of all cancers combined and cancer at 19 specific sites. Over a median follow-up of 12.0 years, 20,928 incident cancers were identified. We used Cox proportional hazards models to estimate HR and 95% confidence intervals (CI) per 10 cm increase in height, with adjustment for established risk factors. We also examined potential effect modification of the association with all cancer and specific cancers.

Results: Height was significantly positively associated with risk of all cancers (HR = 1.13; 95% CI, 1.11–1.16), as well as with cancers of the thyroid, rectum, kidney, endometrium, colorectum, colon, ovary, and breast, and with multiple myeloma and melanoma (range of HRs: 1.13 for breast cancer to 1.29 for multiple myeloma and thyroid cancer). These associations were generally insensitive to adjustment for confounders, and there was little evidence of effect modification.

Conclusions: This study confirms the positive association of height with risk of all cancers and a substantial number of cancer sites.


The Taller the Woman, the Greater the Cancer Risk?

Taller postmenopausal women face higher risks for 10 types of cancer, according to a study in Cancer Epidemiology, Biomarkers and Prevention.

Researchers examined the association between height and cancer risk among some 145,000 Women’s Health Initiative participants. During roughly 12 years of follow-up, 14% received diagnoses of invasive cancer.

After multivariable adjustment, the risk for all cancers increased significantly, by 13%, with each 10-cm (4-inch) increase in height. In particular, risks for the following types of cancer were increased: breast, colon, colorectal, endometrial, melanoma, multiple melanoma, ovarian, rectal, renal, and thyroid. Additional adjustment for cancer screening did not alter the results.

The researchers say height should be considered “a marker for one or more exposures that influence cancer risk rather than a risk factor itself.”

Source:Cancer Epidemiology, Biomarkers & Prevention 


Positive Outlook Linked to Reduction in Cardiac Events Such as Heart Attacks.

Story at-a-glance

  • People who reported being cheerful, relaxed, satisfied with life and full of energy had a one-third reduction in coronary events like a heart attack, according to new research
  • Those with the highest risk of coronary events enjoyed an even greater risk reduction of nearly 50 percent
  • All of your feelings, positive or negative, create physiological changes; stress, for instance, is increasingly being viewed as a cardiovascular risk marker
  • It’s not always easy, but you actually can choose to be happy and more optimistic — and enjoy significant health benefits as a result


Having a positive outlook and a cheerful disposition isn’t only a happier way to live your life – it’s a healthier way as well.

The connection between optimism and other positive emotions and good health has been firmly established by scientific research, and the link appears to be particularly strong when it comes to heart health. Being lighthearted, it turns out, is one of the best ways to protect your heart.

Positive Well-Being Reduces Heart Attack and Other Coronary Events by One-Third

In a study of nearly 1,500 people with an increased risk of early-onset coronary artery disease, those who reported being cheerful, relaxed, satisfied with life and full of energy had a one-third reduction in coronary events like a heart attack.

Those with the highest risk of coronary events enjoyed an even greater risk reduction of nearly 50 percent. This was true even when other heart disease risk factors, such as smoking, age and diabetes, were taken into account. The study’s lead author noted:1

“If you are by nature a cheerful person and look on the bright side of things, you are more likely to be protected from cardiac events. A happier temperament has an actual effect on disease and you may be healthier as a result.”

This is but one study to find a strong connection between positive psychological well-being and cardiovascular (and overall) health. Separate research has similarly found:

  • Positive psychological well-being is associated with a consistent reduced risk of coronary heart disease (CHD)2
  • Emotional vitality may protect against risk of CHD in men and women3
  • Cheerful heart disease patients live longer than pessimistic heart patients4
  • Very optimistic people have lower risks of dying from any cause, as well as lower risks of dying from heart disease, compared to highly pessimistic people5

Why Is Positive Well-Being Protective to Your Heart?

Every one of us will encounter personal tragedies in our lives. Applying the inverse paranoid principle, as taught by W. Clement Stone, has been a guiding helpful principle for me for many years to help address life’s challenges. Admittedly, it isn’t always easy, but the benefits are profound.

Unlike a conventional paranoid who believes the world is out to get him, an inverse paranoid believes the opposite: that every awful tragedy that befalls you ultimately is for some purpose that will benefit you far more than you can possibly imagine, even if you are unable to see it at the time.

There are several theories why a positive outlook is protective for your heart, including that happier people may take better care of themselves and be more likely to lead healthier lifestyles overall. However, at least one of the studies above accounted for these differences and still found optimism to be protective.

It’s likely that positive mood exerts some type of beneficial biological changes in your body, but researchers aren’t yet sure exactly what they are. At least part of the answer likely has to do with stress, or rather, lower levels of it in people who are more optimistic.

All of your feelings, positive or negative, come with corresponding physiological changes. Your skin, heart rate, digestion, joints, muscle energy levels, the hair on your head, and countless cells and systems you don’t even know about change with every emotion.

Stress plays a major role in your immune system, and can impact your blood pressure, cholesterol levels, brain chemistry, blood sugar levels, and hormonal balance. It can even “break” your heart, and is increasingly being viewed as a cardiovascular risk marker. So regular stress relief is imperative to protecting your heart health.

Extreme Stress Is Linked to Heart Problems

Mounting research shows that people exposed to traumatic and/or long-term stressors, such as combat veterans, New Orleans residents who went through Hurricane Katrina, and Greeks struggling through financial turmoil, have higher rates of cardiac problems than the general population.

Several such studies were recently discussed at the 2013 American College of Cardiology conference in San Francisco. In one study, which involved nearly 208,000 veterans aged 46 to 74, 35 percent of those diagnosed with post-traumatic stress disorder (PTSD) developed insulin resistance in two years, compared to only 19 percent of those not diagnosed with PTSD.6

Insulin resistance can lead to type 2 diabetes and hardening of the arteries. PTSD sufferers also had higher rates of metabolic syndrome — a collection of risk factors that raise your risk of heart disease, such as high body fat, cholesterol, blood pressure and blood sugar levels. More than half (about 53 percent) of veterans with PTSD had several of these symptoms, compared to 37 percent of those not suffering with PTSD.

Extreme grief, regardless of the cause, can actually “break” your heart as well. In comparing how grief affects your heart disease risk within a period of time, researchers found that losing a significant person in your life raises your risk of having a heart attack the next day by 21 times, and in the following week by 6 times.7 The risk of heart attacks began to decline after about a month had passed, perhaps as levels of stress hormones begin to level out.

The featured study’s author suggested that you are born with a certain temperament, and if you’re not naturally a positive person it can be difficult to change your personality into someone who is. I tend to disagree, however. It’s not always easy, but you can choose to be happy, and in the vast majority of circumstances there’s no one who can stop you except for yourself. David Kekich, founder of the Maximum Life Foundation, recommends the following seven steps to increase the quality and quantity of your life. I invite you to listen to my interview with David, above, for more details.

1. Appropriate diet
2. Exercise
3. Sensible supplementation
4. Lifestyle habits such as quitting smoking and maintaining a healthy weight
5. Seeing an anti-aging physician
6. Stress management
7. Attitude/positive thoughts

22 Secrets of Happy People

The truth is, happiness doesn’t come from wealth, perfect looks or even a perfect relationship. Happiness comes from within. This is why, if you truly want to be happy, you need to work on yourself, first. And the health benefits mentioned above, like a significantly reduced risk of heart attack and other cardiac events, should provide ample motivation for doing so. Those who are happy tend to follow a certain set of habits that create peace in their lives; if you learn to apply these habits in your own life, there’s a good chance you’ll be happier too.

1. Let go of grudges 2. Treat everyone with kindness 3. Regard your problems as challenges
4. Express gratitude for what you have 5. Dream big 6. Don’t sweat the small stuff
7. Speak well of others 8. Avoid making excuses 9. Live in the present
10. Wake up at the same time every morning 11. Don’t compare yourself to others 12. Surround yourself with positive people
13. Realize that you don’t need others’ approval 14. Take time to listen 15. Nurture social relationships
16. Meditate 17. Eat well 18. Exercise
19. Live minimally 20. Be honest 21. Establish personal control
22. Accept what cannot be changed