Risk factor

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

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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

positive

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    

Source: mercola.com

A Heart-Failure Prevention Strategy Put to the Test.

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An intervention based on biomarker screening yields improved rates of left ventricular dysfunction but uncertain clinical benefit.
The prevalence of heart failure (HF) is rising, despite progress in understanding and treating risk factors. In a nonblinded trial, 1374 adults (average age, 65; 45% men) with ≥1 risk factor for HF (≥3, 27%) underwent annual B-type natriuretic peptide (BNP) screening and were randomized to either BNP-guided intervention or usual care, in which BNP results were unavailable to providers. Intervention-group participants with elevated BNP levels (≥50 pg/mL) were referred for echocardiography and collaborative specialist–primary care. The primary endpoint was the composite of new-onset HF and left ventricular (LV) systolic dysfunction, with or without symptoms; because of slower-than-anticipated enrollment, LV diastolic dysfunction was added to the composite endpoint after trial inception.

During mean follow-up of 4.2 years, the revised primary endpoint occurred significantly less frequently in the intervention group than in the usual-care group (5.3% vs. 8.7%; odds ratio, 0.55). The rate of asymptomatic LV dysfunction was also lower in the intervention group (4.3% vs. 6.6%; OR, 0.57; P=0.01). The risk for symptomatic HF did not differ significantly between the two groups (1.0% vs. 2.1%; OR, 0.48; P=0.12), but the risk for emergency cardiovascular hospitalization was significantly lower in the intervention group (22.3 vs. 40.4 per 1000 patient-years). Of note, renin-angiotensin-aldosterone–inhibitor use was more common in the intervention group than in the usual-care group (56.5% vs. 49.6%).

COMMENT

This study is important as a relatively rigorous attempt to assess a preventive strategy for heart failure, but the results should not change practice. The lack of blinding could explain some of the outcome differences; the importance of asymptomatic left ventricular dysfunction — especially echocardiographic diastolic abnormalities — is of questionable importance to patients; and the feasibility of implementing the intervention in large populations remains unclear. Nonetheless, these findings should initiate a robust discussion about HF prevention, including the value of biomarkers for this purpose.

 

Source: NEJM

 

Pre-eclampsia and the risk of kidney disease.

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Worldwide, about 2—8% of pregnancies are complicated by pre-eclampsia, a disorder that is characterised by new-onset hypertension and proteinuria after 20 weeks of pregnancy.1 Pre-eclampsia is associated with risk of adverse fetal outcomes and can progress to severe pre-eclampsia, eclampsia, or death if not diagnosed and treated with delivery. Substantial progress in understanding the pathophysiological mechanisms of the disease has been made in recent years, and changes in concentrations of soluble fms-like tyrosine kinase 1 and other angiogenic factors seem to be key.2 However, mechanisms behind pre-eclampsia and development of acute kidney injury and chronic kidney disease in the mother are less well understood and warrant further discussion.

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Although acute kidney injury caused by pre-eclampsia or eclampsia is rare in high-income countries, it complicates 2% of third-trimester pregnancies in India, for example, with pre-eclampsia accounting for 36% of cases (ie, pre-eclampsia associated with acute kidney injury might occur in one of 150 pregnancies).3 Dialysis might be required in up to 50% of cases, and when not available, acute kidney injury is a frequent cause of maternal death. Other major causes of acute kidney injury associated with pregnancy in developing countries include sepsis and major bleeding, whereas less common disorders such as primary renal disease, thrombotic thrombocytopenic microangiopathy, or acute fatty liver of pregnancy are probably relatively more common in developed countries. Although most women with acute kidney injury in pregnancy recover renal function, 7—29% do not fully recover, which can have serious long-term outcomes.3, 4 However, few high-quality studies have assessed the cause, prevalence, and prognosis of acute kidney injury in pregnancy, and more studies are needed to inform strategies for prevention, treatment, and follow-up.

Despite several small studies showing recovery of renal function after so-called pure pre-eclampsia,4 a population-based study from Norway suggested that women who had had pre-eclampsia were at a four-to-five-times increased risk of development of end-stage renal disease during a follow-up of 35 years.5 The risk was significant after exclusion of women with known kidney disease, diabetes, hypertension, or rheumatic disease before pregnancy. Other studies6, 7 showed that pre-eclampsia was a significant risk marker for development of kidney disease, requiring a diagnostic kidney biopsy, but that previous pre-eclampsia was not associated with rapid progression of established kidney disease to end-stage renal disease, suggesting that pre-eclampsia is more strongly associated with the development of kidney disease than with subsequent progression. A Taiwanese study8 also noted an increased risk of chronic kidney disease and end-stage renal disease in women with previous pre-eclampsia. In line with these findings, a meta-analysis concluded that women with previous pre-eclampsia had a four-times increased risk of microalbuminuria 5—10 years after a pre-eclamptic pregnancy compared with women without previous pre-eclampsia.9 This meta-analysis was, however, restricted by inclusion of small studies of variable quality and most of the women either had severe pre-eclampsia or underlying disease such as diabetes mellitus. Associations between pre-eclampsia and subsequent microalbuminuria, which suggest renal injury resulting from pre-eclampsia, need to be verified in large population-based studies.

How pre-eclampsia predisposes to an increased risk of renal disease is not well understood. The issue is complicated by the strong association between pre-eclampsia and cardiovascular risk factors, which also increase risk of kidney disease. That pre-eclampsia might induce primary renal injury is, however, supported by reports that the risk of kidney disease and microalbuminuria after pre-eclampsia seems to be greater than the risk of cardiovascular disease.5, 9, 10 In addition, much the same increase in risk was noted for all types of kidney disease after pre-eclampsia,5, 6 underscoring the hypothesis that a primary renal insult, possibly mediated by extensive endothelial or podocyte injury,11 induces nephron loss and contributes to progression of renal disease. The strong clinical similarity between pre-eclampsia and underlying kidney disease also complicates these studies, because the clinical presentations can be almost identical, especially in multiparous women.12

Developmental and genetic factors are also important determinants of pre-eclampsia risk (as discussed in the accompanying Series), and might themselves be independent risk factors for renal disease. Men and women born in pre-eclamptic pregnancies are at an increased risk of fathering or bearing pre-eclamptic pregnancies, respectively,13 and women born with low birthweight had a 1·5-fold increased risk of pre-eclampsia.14 This intergenerational transfer of risk might suggest genetic predisposition, perinatal programming, or socioeconomic factors, the last of which is an independent risk factor for pre-eclampsia, especially in developing countries.15

Pre-eclampsia is probably an important cause of acute kidney injury and an important risk marker for subsequent chronic kidney disease. Women with previous pre-eclampsia should receive long-term follow-up, especially with respect to hypertension, insulin resistance, and obesity. However, pre-eclampsia might also unmask underlying primary renal disease, and women with pre-eclampsia should be monitored for proteinuria and hypertension within 6—8 weeks of delivery and have a nephrological work-up if these disorders do not resolve.

References

1 Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet 2010; 376: 631-644. Summary | Full Text |PDF(865KB) | CrossRef | PubMed

2 Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med 2004; 350: 672-683. CrossRef | PubMed

3 Prakash J, Niwas SS, Parekh A, et al. Acute kidney injury in late pregnancy in developing countries. Ren Fail 2010; 32: 309-313.CrossRef | PubMed

4 Sibai BM, Villar MA, Mabie BC. Acute renal failure in hypertensive disorders of pregnancy. Pregnancy outcome and remote prognosis in thirty-one consecutive cases. Am J Obstet Gynecol 1990; 162: 777-783. CrossRef | PubMed

5 Vikse BE, Irgens LM, Leivestad T, Skjaerven R, Iversen BM. Preeclampsia and the risk of end-stage renal disease. N Engl J Med2008; 359: 800-809. CrossRef | PubMed

6 Vikse BE, Irgens LM, Bostad L, Iversen BM. Adverse perinatal outcome and later kidney biopsy in the mother. J Am Soc Nephrol2006; 17: 837-845. CrossRef | PubMed

7 Vikse BE, Hallan S, Bostad L, Leivestad T, Iversen BM. Previous preeclampsia and risk for progression of biopsy-verified kidney disease to end-stage renal disease. Nephrol Dial Transplant 2010; 25: 3289-3296. CrossRef | PubMed

8 Wang IK, Muo CH, Chang YC, et al. Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ 2013; 185: 207-213. CrossRef | PubMed

9 McDonald SD, Han Z, Walsh MW, Gerstein HC, Devereaux PJ. Kidney disease after preeclampsia: a systematic review and meta-analysis. Am J Kidney Dis 2010; 55: 1026-1039. CrossRef | PubMed

10 Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta-analysis. BMJ 2007; 335: 974. CrossRef | PubMed

11 Garovic VD, Wagner SJ, Turner ST, et al. Urinary podocyte excretion as a marker for preeclampsia. Am J Obstet Gynecol 2007;196: 320. PubMed

12 Fisher KA, Luger A, Spargo BH, Lindheimer MD. Hypertension in pregnancy: clinical-pathological correlations and remote prognosis. Medicine (Baltimore) 1981; 60: 267-276. PubMed

13 Skjaerven R, Vatten LJ, Wilcox AJ, Ronning T, Irgens LM, Lie RT. Recurrence of pre-eclampsia across generations: exploring fetal and maternal genetic components in a population based cohort. BMJ 2005; 331: 877. CrossRef | PubMed

14 Rasmussen S, Irgens LM. Pregnancy-induced hypertension in women who were born small. Hypertension 2007; 49: 806-812.CrossRef | PubMed

15 Nanjundan P, Bagga R, Kalra JK, Thakur JS, Raveendran A. Risk factors for early onset severe pre-eclampsia and eclampsia among north Indian women. J Obstet Gynaecol 2011; 31: 384-389. CrossRef | PubMed

Source: Lancet

Mediators of the association between pre-eclampsia and cerebral palsy: population based cohort study.

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Abstract

Objective To test the hypothesis that pre-eclampsia is a risk factor for cerebral palsy mediated through preterm birth and being born small for gestational age.

Design Population based cohort study.

Setting Clinical data from the Norwegian Cerebral Palsy Registry were linked with perinatal data prospectively recorded by the Medical Birth Registry of Norway.

Participants All singleton babies who survived the neonatal period during 1996-2006 (849 children with cerebral palsy and 616 658 control children).

Main outcome measures Cerebral palsy and cerebral palsy subtypes.

Results Children exposed to pre-eclampsia had an excess risk of cerebral palsy (unadjusted odds ratio 2.5, 95% confidence interval 2.0 to 3.2) compared with unexposed children. Among children born at term (≥37 weeks), exposure to pre-eclampsia was not associated with an excess risk of cerebral palsy in babies not born small for gestational age (1.2, 0.7 to 2.0), whereas children exposed to pre-eclampsia and born small for gestational age had a significantly increased risk of cerebral palsy (3.2, 1.5 to 6.7). Non-small for gestational age babies born very preterm (<32 weeks) and exposed to pre-eclampsia had a reduced risk of cerebral palsy compared with unexposed children born at the same gestational age (0.5, 0.3 to 0.8), although the risk was not statistically significantly reduced among children exposed to pre-eclampsia and born small for gestational age (0.7, 0.4 to 1.3). Exposure to pre-eclampsia was not associated with a specific cerebral palsy subtype.

Conclusions Exposure to pre-eclampsia was associated with an increased risk of cerebral palsy, and this association was mediated through the children being born preterm or small for gestational age, or both. Among children born at term, pre-eclampsia was a risk factor for cerebral palsy only when the children were small for gestational age.

Discussion

In this study we found that pre-eclampsia was associated with an increased risk of cerebral palsy and that the excess risk was mainly mediated through preterm birth, but also through being born small for gestational age. Exposed children born at term as non-small for gestational age did not have an excess risk of cerebral palsy and we did not find that a specific cerebral palsy subtype was more common in children exposed to pre-eclampsia than not exposed. Thus we were not able to find evidence for a direct effect of pre-eclampsia on the risk of cerebral palsy.

What is already known on this topic

  • Pre-eclampsia is a frequent cause of preterm birth and being born small for gestational age, both of which are known risk factors for cerebral palsy
  • Observational studies have shown conflicting results with respect to whether pre-eclampsia is a risk factor for cerebral palsy
  • Pre-eclampsia is a risk factor for cerebral palsy mainly mediated through preterm birth and being small for gestational age
  • Among term born children exposed to pre-eclampsia only those born small for gestational age had an excess risk of cerebral palsy
  • Pre-eclampsia was not associated with specific subtypes of cerebral palsy

What this study adds

 

Source: BMJ

 

Respiratory infections may increase infants’ risk for diabetes.

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Respiratory infections in early childhood, especially in the first year of life, may be a risk factor for the development of type 1 diabetes, according to data.

In a prospective cohort study conducted in Munich, researchers examined data for 148 children at high risk for developing type 1 diabetes with documentation of 1,245 infectious events in 90,750 person-days during their first 3 years of life. Documentation was collected from the ongoing BABYDIET study, a German dietaryintervention study that tests the effects of delayed gluten exposure on the development of islet autoimmunity in children at increased risk for diabetes, researchers wrote.

The HR for islet autoantibody seroconversion associated with respiratory infections was increased during the first 6 months of life (HR=2.27; 95% CI, 1.32-3.91) and for those aged 6 to 11.9 months (HR=1.32; 95% CI, 1.08-1.61).

According to data, a higher number of respiratory infections were reported in the 6 months before islet autoantibody seroconversion and also were associated with an increased HR (HR=1.42; 95% CI, 1.12-1.80), the researchers wrote.

“While there were no islet autoantibody seroconversion events observed in the first 6 months of life, the incidence rates of seroconversion per 100 person-years were 8.51 in the second-half year, 4.07 in the second year, and 3.67 in the third year of life. The mean incidences of the three infection categories also increased considerably after the first 6 months of life and remained relatively constant thereafter, with a slight decline in the third year of life,” researchers wrote.

Besides these findings, there is some evidence connecting short-term effects of infectious events and the development of autoimmunity, they wrote.

Source: Endocrine Today

 

 

Primary prevention of cardiovascular disease: new guidelines, technologies and therapies.

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Abstract

  • A trend in primary prevention of cardiovascular disease (CVD) has been a move away from managing isolated risk factors, such as hypertension and dyslipidaemia, towards assessment and management of absolute CVD risk.
  • In Australian guidelines, absolute CVD risk is calculated as the probability of a stroke, transient ischaemic attack, myocardial infarction, angina, peripheral arterial disease or heart failure occurring within the next 5 years.
  • Absolute CVD risk should be regularly assessed in patients aged 45 years or older (35 years or older in Aboriginal and Torres Strait Islander people) using the Australian absolute CVD risk calculator (http://www.cvdcheck.org.au).
  • For patients currently taking a blood pressure (BP)-lowering or lipid-lowering agent, pretreatment values should be used to calculate risk.
  • Patients at high absolute risk of CVD (> 15% over 5 years) should be treated with both BP-lowering and lipid-lowering agents, unless contraindicated or clinically inappropriate.
  • For patients at moderate absolute risk of CVD (10%–15%) treatment with a BP-lowering and/or a lipid-lowering agent should be considered if the risk remains elevated after lifestyle interventions, BP is ≥ 160/100 mmHg, there is a family history of premature CVD, or the patient is of South Asian, Middle Eastern, Maori, Pacific Islander, Aboriginal or Torres Strait Islander ethnicity.
  • BP measurements taken using an oscillometric device can be used to approximate mean daytime ambulatory BP.
  • Conclusion
  • The move to an approach based on absolute risk for the primary prevention of CVD is likely to improve the effectiveness and cost-effectiveness of treatment, and the 2009 and 2012 NVDPA guidelines support this approach. The absolute risk approach targets the patients who are most likely to benefit from medication, and reduces the medicalisation of patients at low risk. The increasing availability of cardiovascular risk calculators, either on the internet or as standalone software, also removes one of the barriers to implementing the absolute risk approach. New technologies have varying evidence of utility, but oscillometric BP devices can be readily adopted. The role of coronary artery calcium scoring and other biomarkers in risk stratification is yet to be established.

Source: MJA

Diet and Physical Activity for the Prevention of Noncommunicable Diseases in Low- and Middle-Income Countries: A Systematic Policy Review.

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Abstract

Background

Diet-related noncommunicable diseases (NCDs) are increasing rapidly in low- and middle-income countries (LMICs) and constitute a leading cause of mortality. Although a call for global action has been resonating for years, the progress in national policy development in LMICs has not been assessed. This review of strategies to prevent NCDs in LMICs provides a benchmark against which policy response can be tracked over time.

Methods and Findings

We reviewed how government policies in LMICs outline actions that address salt consumption, fat consumption, fruit and vegetable intake, or physical activity. A structured content analysis of national nutrition, NCDs, and health policies published between 1 January 2004 and 1 January 2013 by 140 LMIC members of the World Health Organization (WHO) was carried out. We assessed availability of policies in 83% (116/140) of the countries. NCD strategies were found in 47% (54/116) of LMICs reviewed, but only a minority proposed actions to promote healthier diets and physical activity. The coverage of policies that specifically targeted at least one of the risk factors reviewed was lower in Africa, Europe, the Americas, and the Eastern Mediterranean compared to the other two World Health Organization regions, South-East Asia and Western Pacific. Of the countries reviewed, only 12% (14/116) proposed a policy that addressed all four risk factors, and 25% (29/116) addressed only one of the risk factors reviewed. Strategies targeting the private sector were less frequently encountered than strategies targeting the general public or policy makers.

Conclusions

This review indicates the disconnection between the burden of NCDs and national policy responses in LMICs. Policy makers urgently need to develop comprehensive and multi-stakeholder policies to improve dietary quality and physical activity.

Discussion

Despite the global disease burden of NCDs in LMICs, policies that address at least one risk factor for NCDs were found in a minority of the LMICs reviewed, and only a handful of them comprehensively tackled NCDs through integrated action on various risk factors. Even if the 24 countries with unknown existence of a NCD prevention policy actually have such a policy, the proportion with countries tackling a risk factor would amount to 56% (78/140). This finding is discouraging, because in 2004, all countries expressed a strong commitment to action to address lifestyle, diet, and physical activity [20]. Our results show that, in spite of that official commitment, most LMICs are poorly prepared to tackle the NCD increase and that little progress has been made in recent years. This finding is consistent with the results of Alwan et al. [23], who reported the results of a survey in 2010 that was limited to countries with high NCD-related mortality.

Most of the policies in our review were poorly accessible and were only obtained after an extensive search or through personal contacts. Such a situation is certainly not favorable for benchmarking and communication of policies. In agreement with Sridhar et al. [88], we argue how better sharing of best practices and lessons learned with regard to policy development is needed to address the current NCD pandemic. Additional instruments and platforms to share lessons learned in policy development and implementation are needed. Policy databases with links to documents were created previously, but are restricted to nutrition action [89] or the European region [26]. An open-access, full-text global repository of initiatives and policies to address NCDs would be a great step forward. It could also contribute to global leadership and shared accountability in the global fight against NCDs, an issue that is long overdue [90]. Ideally, such a policy database would be connected to surveillance data on the main NCD risk factors, as suggested previously [23], and would facilitate tracking progress in the coming years. We are ready to organize such an open-access repository and invite interested policy makers to contact us for an update of the current database.

Priority setting and clear articulation of what needs to be done by stakeholders is a second key issue that emerged in this analysis. Countries seasoned in the fight against NCDs develop comprehensive strategies that focus on critical risk factors and what is expected of stakeholders [91]. In the present analysis, the level of detail and outlining of the organization of policy actions to undertake was generally discouraging. Only a minority of the policies reviewed surpassed description of policy actions and included a budget, implementation plan, time frame, and devolvement of responsibility for strategies to combat specific risk factors. Various policies describe strategies and actions for NCD prevention as “the need to develop and review dietary guidelines and recommendations for people suffering from nutrition-related NCDs” or use generic statements such as “create awareness of healthy eating lifestyle to control NCDs.” Such general statements are not informative, and clear actions need to be outlined in the policies to mobilize stakeholders for effective action [92].

Since its inception during the 1992 International Conference on Nutrition [93], the approach to streamline nutrition action in national policies has had limited success, partly because of the lack of strong leadership and commitment to lead concerted action involving various stakeholders [94]. The current scientific evidence and international experience in the fight against NCDs consistently indicates the need for comprehensive and integrated action on various risk factors [95]. Mobilization of the main actors—in particular, governments, international agencies, the private sector, civil society, health professionals, and individuals—is imperative [96]. An important limitation of most policies included in the analysis is the absence of plans, mechanisms, and incentives to foster multi-stakeholder and cross-sector collaboration. The food and nonalcoholic beverage industry, for instance, can play a role in the promotion of healthier lifestyles. However, before engaging with the private sector, government agencies should be aware of the need to manage potential conflicts of interest between the government and the private sector and should try to address these by defining clear roles, responsibilities, and targets to be achieved as a result of their collaboration [97]. Most strategies encountered in the policies were directed towards government agencies and consumers, and few were targeted at the business community, international agencies, or civil society. The United Nations Political Declaration on NCDs makes a strong call for multi-stakeholder partnerships to be leveraged for effective prevention of NCDs. Policy makers in LMICs may need additional support for the development of multi-stakeholder collaborations to address the burden imposed by NCDs as well as their root causes.

In our review of governmental policies relating to NCD prevention in LMICs, strategies to increase fruit and vegetable intake were the most frequent dietary action for NCD prevention. This is hardly surprising, as fruit and vegetable interventions were taken up early on in LMICs, primarily to address prevailing micronutrient deficiencies such as vitamin A deficiency [98]. Many of these experiences, however, are restricted to the development of food-based dietary guidelines or incentives targeted towards the agricultural sector. Policy measures to achieve better diet will require constructively engaging much more with a wider range of stakeholders, in particular the food industry, retail, and the catering sector [99]. The difficulty of developing a comprehensive policy response and integrated package of strategies is not restricted to NCDs alone, and has previously been observed in an in-depth analysis of high-burden countries for child malnutrition [100]. We also note that various countries have developed strategies to reduce total fat intake, despite convincing evidence that it is the reduction of saturated and trans-fatty acids in particular, and not total fat intake, that is effective to address NCDs [101].

Most strategies encountered in the policy documents focused on consumers and aimed to prevent NCDs through awareness creation, education (i.e., labeling), or changing individuals’ behavior. The traditional approach to addressing lifestyle changes in individuals has met with very limited success. It is widely accepted that the environmental context drives individual diets and lifestyle [102] and that programs need to incorporate environmental determinants (i.e., the quantity, quality, or price of dietary choices, or the built environment for physical activity) in order to be effective. Such policy measures, in particular those addressing the private sector, were poorly elaborated in the policy documents [103].

A key issue is the actual implementation of policy measures in relation to what was articulated in the documents. The findings of this review indicate that few LMICs have made significant steps in the development of a comprehensive set of strategies to address NCDs. Although an in-depth evaluation of actual implementation, effects, and resources allocated has not been opportune to date, we hope that our findings provide baseline data and encourage countries to develop monitoring and evaluation mechanisms to assess policy response in due time. Documenting the effectiveness of population-based NCD prevention policies will be a critical factor of success to ensure effective action in LMICs [4].

For this review, we were able to assess documents in all languages received. Because of language constraints, however, two of the documents [74],[87] were coded by only one researcher. To assess the content of the policy of Iran, we relied on translations by experienced senior Iranian researchers. All other policy documents were obtained in Spanish, Portuguese, French, or English and were analyzed accordingly by the research team. For China and the Russian Federation, appropriate English versions of the policies were obtained from the Chinese Centers for Disease Control and the United States Department of Agriculture, respectively. Despite indications of availability of relevant policies in the European region [26], language limitations did not allow us to search the websites of a number of countries such as Azerbaijan, Belarus, and the Russian Federation.

The restriction of our review to only national policies presents a number of limitations. The mere presence or absence of policies or strategies for NCDs in a policy document does not necessarily reflect concrete action. Conversely, nutritional interventions have been implemented in some countries without a policy being developed and published [104]. In addition, this review assessed the contents of the policy documents as they were published and did not capture local or regional activities, or initiatives that emerged after the publication of the policies. The findings from a survey in countries with a high burden of NCDs, such as Thailand and South Africa, illustrate this discrepancy [23]. The contents might have been modified over time in response to new scientific findings, emerging nutritional challenges, or changes in the countries’ priorities [91]. In addition, it is important to point out that we extracted only actions that explicitly referred to one of the risk factors analyzed. Generic statements such as “development of food-based dietary guidelines” or “establishment of fiscal measures for a healthy diet” were hence not coded.

The present review shows that the policy response to address current NCD challenges through diet and physical inactivity in LMICs is inadequate since endorsement of the Global Strategy on Diet, Physical Activity and Health [20]. LMICs urgently need to scale up interventions and develop integrated policies that address various risk factors for NCD prevention through multi-stakeholder collaboration and cross-sector involvement. Clear and prioritized actions are needed to harness the NCD epidemic. Such actions need to be documented in policy documents that are publicly available to share lessons learned, promote engagement with the stakeholders, and stimulate accountability and leadership in the fight against the burden of NCDs in LMICs. The establishment of an open-access and publicly accessible database of policy documents with regular systematic reviews of policy development might prove to be an incentive in this regard.

Source: PLOS

 

 

 

Extreme Bilirubin Levels as a Causal Risk Factor for Symptomatic Gallstone Disease.

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Importance  In individuals without blockage of their bile ducts, levels of plasma bilirubin likely reflect levels of biliary bilirubin; higher biliary bilirubin levels may increase the risk of gallstone disease.

Objective  To test the hypothesis that a lifelong increase in plasma bilirubin levels is a causal risk factor for symptomatic gallstone disease in the general population.

Design, Setting, and Participants  In a prospective study of the Danish general population (N = 61 212), we first tested whether elevated levels of plasma bilirubin predicted greater risk of symptomatic gallstone disease. Second, taking advantage of mendelian randomization, we tested whether a genetic variant in the bilirubin glucoronidating enzyme UGT1A1 (rs6742078) was associated with increased plasma bilirubin levels and, in turn, with an increased risk of symptomatic gallstone disease.

Main Outcomes and Measures  Plasma bilirubin level and symptomatic gallstone disease.

Results  During 34 years of follow-up, 3374 individuals developed symptomatic gallstone disease. In adjusted analyses, persons with plasma bilirubin levels in the 10th decile had a greater risk of symptomatic gallstone disease compared with those with plasma bilirubin levels in deciles 1 through 9; the hazard ratios (HRs) (95% CIs) were 1.57 (1.26-1.96) overall, 1.36 (1.02-1.82) in women, and 2.00 (1.41-2.83) in men. UGT1A1 genotype explained 20% of the total variation in plasma bilirubin levels and was associated with increases in the mean plasma bilirubin level overall of +16% (+0.09 mg/dL) in GT heterozygotes and +90% (+0.50 mg/dL) in TT homozygotes compared with GG homozygotes, with similar effects in women and men (P for trend <.001 for all). The corresponding HRs (95% CIs) for symptomatic gallstone disease were 1.09 (1.02-1.17) for GT heterozygotes and 1.22 (1.09-1.36) for TT homozygotes vs GG homozygotes and similar in women and men (P for trend = .04-<.001).

Conclusions and Relevance  These results are compatible with a causal association between extreme levels of plasma bilirubin and increased risk of symptomatic gallstone disease.

Source: JAMA

 

Risk Factors for Bronchiectasis in Children with Cystic Fibrosis.

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BACKGROUND

Bronchiectasis develops early in the course of cystic fibrosis, being detectable in infants as young as 10 weeks of age, and is persistent and progressive. We sought to determine risk factors for the onset of bronchiectasis, using data collected by the Australian Respiratory Early Surveillance Team for Cystic Fibrosis (AREST CF) intensive surveillance program.

METHODS

We examined data from 127 consecutive infants who received a diagnosis of cystic fibrosis after newborn screening. Chest computed tomography (CT) and bronchoalveolar lavage (BAL) were performed, while the children were in stable clinical condition, at 3 months and 1, 2, and 3 years of age. Longitudinal data were used to determine risk factors associated with the detection of bronchiectasis from 3 months to 3 years of age.

RESULTS

The point prevalence of bronchiectasis at each visit increased from 29.3% at 3 months of age to 61.5% at 3 years of age. In multivariate analyses, risk factors for bronchiectasis were presentation with meconium ileus (odds ratio, 3.17; 95% confidence interval [CI], 1.51 to 6.66; P=0.002), respiratory symptoms at the time of CT and BAL (odds ratio, 2.27; 95% CI, 1.24 to 4.14; P=0.008), free neutrophil elastase activity in BAL fluid (odds ratio, 3.02; 95% CI, 1.70 to 5.35; P<0.001), and gas trapping on expiratory CT (odds ratio, 2.05; 95% CI, 1.17 to 3.59; P=0.01). Free neutrophil elastase activity in BAL fluid at 3 months of age was associated with persistent bronchiectasis (present on two or more sequential scans), with the odds seven times as high at 12 months of age and four times as high at 3 years of age.

 

CONCLUSIONS

Neutrophil elastase activity in BAL fluid in early life was associated with early bronchiectasis in children with cystic fibrosis. 

Source: NEJM

 

Does Cracking Your Knuckles Cause Arthritis?.

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knuckle-crack

 

Do you crack or “pop” your knuckles? Some believe it may cause, or worsen, joint conditions such as arthritis. However, according to the featured research,1, 2knuckle-cracking does not appear to be a risk factor for osteoporosis in that joint.

About one in five adults, or nearly 50 million Americans, have been diagnosed with arthritis, the most common form of which is osteoarthritis.3

If you have osteoarthritis, the cartilage within your joints is progressively being damaged, and the synovial fluid that keeps your joints lubricated and cushioned is typically reduced as well.

The pain and joint stiffness that you feel is a result of your bones starting to come into contact with each other as cartilage and synovial fluid is reduced, and if you don’t take action, it can become progressively worse until you are unable to carry out your normal daily activities.

In conclusion, the authors stated that:

“Total past duration (in years) and volume (daily frequency ‘- years) of knuckle-cracking (KC) of each joint type also was not significantly correlated with OA at the respective joint. A history of habitual KC – including the total duration and total cumulative exposure ‘does not seem to be a risk factor for hand OA.'”

Twenty years ago, I co-authored a paper titled “Cracking down on ‘neck cracking,’ which was published in the journal American Family Physician.4 In it, I argued that self-manipulation can lead to lax ligaments. Personally, I don’t think it’s wise to crack your joints on a regular basis, even if it doesn’t directly lead to arthritis of the joint. That said, what can make arthritis worse, and how can you address arthritic conditions?

What’s the Difference Between Osteoarthritis and Rheumatoid Arthritis?

Osteoarthritis usually occurs in older individuals, but can also be caused by repetitive stress or acute trauma. Rheumatoid arthritis, on the other hand, can affect you at any age, including children. Fortunately, juvenile rheumatoid arthritis (JRA) is relatively rare.

Understanding the differences between the two types of arthritis will help you distinguish which one you have.

Osteoarthritis – Degenerative joint disease usually affects the distal joints, or the joints at the end of your fingers and toes, not the middle ones. Additionally, it’s not symmetrical, so typically you may have it on just one joint, or on one hand or foot and not the other.

Rheumatoid arthritis – RA, on the other hand, is an autoimmune disease that causes your body to break itself down. Therefore, it tends to be bilateral and symmetrical, meaning it’s the same on both sides of your body. If you only have a specific joint affected on one side of your body, it is far less likely to be RA. It also affects your middle joints, and is associated with joint deformities, especially your hands and fingers. It can be very crippling, and people do die from rheumatoid arthritis, so it’s not something to be treated lightly.

Little-Known Risk Factors for Rheumatoid Arthritis and Osteoarthritis

Recent research5 has identified several lifestyle factors and pre-existing conditions that may increase your risk of developing rheumatoid arthritis, including:

  • Smoking
  • Obesity
  • Diabetes

As for osteoarthritis, a recent analysis6 found that the greater a woman’s exposure to perfluorinated compounds (PFCs), the greater her risk for developing osteoarthritis. Interestingly, the same correlation was not found in men. It’s believed the reason for this is the impact of these chemicals on women’s hormones. PFC’s are commonly found in nonstick cookware, takeout containers and carpeting, just to name a few.

Even though osteoarthritis and rheumatoid arthritis are two entirely different diseases, they can be treated in much the same way as foundationally inflammation as at the core of the pain. So even though osteoarthritis is typically caused by wear-and-tear on your joints due to lifestyle, diet and aging, and rheumatoid arthritis is an autoimmune disease in which your body starts destroying itself, you may gain relief from the following treatments regardless of which type of arthritis you have.

First: Basic Lifestyle Changes to Address Arthritis

I believe improving your diet using my nutritional guidelines is crucial for your success. It addresses all of the nutritional guidelines presented in this article, and more. In addition, there are some general principles that seem to hold true for virtually everyone and these include:

  • Eliminating sugar, especially fructose, and most grains. For most people with rheumatoid arthritis, you’ll want to be very careful to limit fructose to just 15 grams per day or less, and this includes fructose from whole fruit.
  • Opting for organic food, preferably locally grown, and eat your food as close to raw as possible
  • Incorporating regular exercise into your daily schedule. Weight training has been found to be of particular benefit for those with rheumatoid arthritis and, contrary to popular belief, if you have osteoarthritis exercise is absolutely crucial to your well-being. Naturally, if you’re in pain, you need to take certain precautions, so for more information on how to adjust your exercise if you have either of these conditions, please follow the links provided

The Importance of Sulfur

Sulfur is just now becoming more widely appreciated as a really critical nutrient, without which many other things don’t work properly, and many are not getting enough sulfur from their diet anymore. Sulfur is found in over 150 different compounds within the human body. There are sulfur components in virtually every type of cell, so it’s extremely important. It plays a critical role in inflammatory conditions such as arthritis, as well as detoxification. Two ways to increase your sulfur intake include:

  • MSM, either from food or supplement: A metabolite of DMSO, MSM primarily impacts your health by reducing inflammation. MSM is 34 percent sulfur by weight, but it’s more than just a simple sulfur donor. It affects sulfur metabolism in your body, although it’s still not entirely clear how. Perhaps most important, MSM helps protect against oxidative damage, and is widely used as a supplement for arthritic conditions.

While many opt for a supplement, MSM is in most raw foods, such as leafy green vegetables. Raw milk has the highest naturally occurring content of MSM.

One caveat is cooking and pasteurization. While MSM is stable to extremes of pH and temperature, it volatilizes and turns to gas very easily. It’s also very water-soluble. So when cooked at high temperatures, it simply wafts off in the steam. That’s why it’s easily removed during cooking and processing. Pasteurization cuts the MSM content by approximately 50 percent. So, in order to ensure you’re getting the most MSM from any food, it must be either raw or as minimally processed as possible.

Fortunately, toxicity studies have shown that MSM is extremely safe and can be taken at very, very high doses. Even if you have a very rich diet full of raw vegetables and MSM-rich foods, you can still supplement and not hit that toxicity level. Clinical research studies have found that the effective amounts range from about 1.5 grams to 6 grams. For comparison, intake of MSM from natural sources such as fruits and vegetables would be in the milligram per day range of about 2.3 to 5.6 mg/day.

  • Bone broth: Simmering leftover bones over very low heat for an entire day will create one of the most nutritious and healing foods known to man. Make sure the bones are from organically raised animals. The connective tissues are sulfur-rich, and when you slow-cook the bones, you dissolve these nutrients out of the bone and into the water.

You can use this broth for soups, stews, or drink it straight. Remember that the “skin” that forms on the top is the best part—this is what contains the most valuable nutrients, including sulfur, along with healthful fats—so make sure to stir it back into the broth.

 

  • Source: mercola.com

 

 

at F�te�� ��� 2 hours before eating them. This will help to get rid of the phytic acid and enzyme inhibitors, which can interfere with the function of your own digestive and metabolic enzymes, in the nuts.  To make them more palatable you can you a dehydrator (I like the Excalibur) to improve the texture.

 

Enzyme inhibitors in nuts (and seeds) help protect the nut as it grows, helping to decrease enzyme activity and prevent premature sprouting. When nuts are soaked, the germination process begins, allowing the enzyme inhibitors to be deactivated and increasing the nutrition of the nut significantly, as well as making them much easier to digest. Macadamia nuts (and other white nuts) have only negligible amounts of enzyme inhibitors, so soaking is not as necessary.

Choose Raw Organic Nuts, Ideally

To increase the positive impacts on your health, look for nuts that are organic and raw, not irradiated or pasteurized. Be aware that pasteurized almonds sold in North America can still be labeled “raw” even though they’ve been subjected to one of the following pasteurization methods:

  • Oil roasting, dry roasting or blanching
  • Steam processing
  • Propylene Oxide (PPO) treatment (PPO is a highly toxic flammable chemical compound, once used as a racing fuel before it was prohibited for safety reasons)

There are generally no truly “raw” almonds sold in North America, so don’t be misled. It is possible to purchase raw almonds in the US, but it has to be done very carefully from vendors selling small quantities that have a waiver from the pasteurization requirement. The key is to find a company with the waiver that is not pasteurizing them.

When consumed with these guidelines in mind, raw, organic nuts are a convenient and enjoyable superfood to add to your diet. And this is precisely why they’re recommended as one of the best sources of healthy fats in my nutrition plan.

Source: mercola.com