Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label cardiovascular mortality. Show all posts
Showing posts with label cardiovascular mortality. Show all posts

Thursday, May 14, 2026

Cardiometabolic diseases remain leading cause of excess American mortality

WOW! Even the Boston University School of Public Health doesn't know that stroke has been called neurological disease by the WHO since 2006 not cardiovascular, once again proving our medical 'professionals' don't keep up to date in their field! Why would your trust anything coming out of such incompetence?

Cardiometabolic diseases remain leading cause of excess American mortality

Between 1999 and 2022, the US had substantially higher death rates than other wealthy nations, largely due to cardiovascular disease, metabolic diseases (including diabetes), Alzheimer's disease and related dementias, and drug and alcohol complications. Policies are needed to address the underlying health, social, and economic conditions that increase Americans' risk of developing these diseases.

Despite having similar access to advanced medical technology, the United States has substantially higher death rates than other high-income countries (HICs), and the gap has been growing for decades. Cardiovascular diseases were the leading cause of excess US deaths, according to a new study led by researchers at Boston University School of Public Health (BUSPH). 

Published in JAMA Network Open, the study found that between 1999-2022, the annual number of excess US deaths-deaths that would not have occurred had the mortality rate in the US been the same as in other HICs-increased steadily through 2019 and then rose rapidly during the COVID-19 pandemic. By 2022, all-cause mortality rates in the US were 38 percent higher than in other HICs. An estimated 12.7 million US deaths could have been averted during this period if US mortality rates mirrored those of its peers. The authors refer to these excess US deaths as "missing Americans."

The study investigated the causes of these excess US deaths, and found that cardiovascular diseases, including heart disease, hypertension, and stroke, were the leading cause of excess mortality nearly every year of this period. Together, cardiovascular and metabolic diseases accounted for over half of all excess US deaths in 2022. Drug poisonings, alcohol-related diseases, and suicides emerged as another major cause of excess mortality during this period, particularly among men and people under 45 years old. Homicide and HIV/AIDS also had mortality rates many times higher in the US than in other HICs; however, these causes were responsible for only a small share of excess US deaths. 

The study builds upon previous findings by the researchers which showed that excess US deaths have increased since 1980 and continued to increase even after the COVID-19 pandemic. The new analysis is the first study to identify all leading causes responsible for these excess US deaths-what the authors refer to as a "population autopsy." Quantifying causes of the US mortality disadvantage can reveal opportunities for intervention, including policies to prevent these fatal conditions from occurring in the first place.

"In public health, we know that death certificates only list the most proximate cause of death and not the full causal chain. Differences in social factors between the US and other HICs can lead to differences in behavioral risk factors, which in turn can lead to higher risks of specific causes of death," says study lead and corresponding author Dr. Jacob Bor, associate professor of global health and epidemiology at BUSPH. "These findings pinpoint the issues that we should be focusing on if we want to address the US mortality disadvantage relative to peer countries."

For the study, Dr. Bor and colleagues from BUSPH, Harvard Medical School, and Hunter College at the City University of New York analyzed US excess deaths by sex, age, and year. They utilized cause-of-death data from the World Health Organization Mortality Database for all deaths occurring from 1999-20222 in the US and 17 other HICs, including Australia, Canada, France, Japan, and the United Kingdom. The team compared excess mortality among the countries used three metrics: excess deaths, which is the difference between reported deaths and deaths that would have occurred if the US had the mortality rate of other HICs; years of life lost, which is the years of potential life lost due to premature deaths; and mortality rate ratios, which compare the risk of different causes of death between the US and other countries. 

Among more than 63.5 million total deaths that occurred during this period, the US experienced an estimated 12,675,646 more excess deaths than would have occurred if their death rates were equal to other HICs. Despite declining between 1999-2009, cardiovascular diseases remained the leading cause of excess deaths during the entire study period, except for 2010, before rising sharply and continuously through 2022. Diabetes, kidney, and metabolic conditions also rose sharply from 2010-2022, following no significant increases from 1999-2009. In 2022, mental health and nervous system disorders such as Alzheimer's disease and other dementias were the leading cause of excess death among people 85 and older. Respiratory illnesses, transportation accidents, and homicides were also major causes of US excess deaths. COVID-19 was a leading cause of US excess deaths from 2020-2022, representing 1 in 5 US excess deaths in 2020 and 2021, and also coinciding with sharp increases in other diseases. 

Importantly, the study findings revealed stark differences in the burden of these causes of deaths, depending on whether they were viewed in absolute or relative terms. For example, in 2022, excess deaths from drug poisonings were 7.48 times higher in the US than in other countries, but only accounted for 10 percent of US excess deaths, while cardiovascular diseases were 1.63 times as high in the US than in other countries, but accounted for 40 percent of US excess deaths.

In US population health research, examining the stagnation in US life expectancy that began in 2010 usually focuses on drug overdoses, alcohol-related deaths, and suicide, known as 'deaths of despair.' One dramatic finding from this study is that on an absolute scale, cardiometabolic diseases are key contributors to the increase in US death rates. If there was one thing we could address on a population scale, tackling cardiometabolic diseases would substantially reduce the US mortality gap with other wealthy nations."

Dr. Andrew Stokes, study senior author, associate professor of global health at BUSPH

Drug poisonings are still a critical component of the US excess death conversation, the researchers note, particularly in terms of years of life lost, as this measure focuses on premature deaths and captures the societal burden of losing young people. These deaths represented the fastest increase in excess US deaths, rising from a near-equivalent level with peer countries in 1999 to more than 130,000 excess deaths in 2022, with a particular rise in 2013 after fentanyl entered the US drug supply. These causes also contributed to excess deaths among people ages 45-65.

The US did outperform peer countries in a couple of categories, comprising fewer excess deaths in 2022 for cancers (excluding lung cancer) and influenza, which Dr. Stokes attributes partly to advancements within the US healthcare system. "We've come a long way with medical innovations to screen and treat cancers," he says.

The team says that more research is needed to understand the sharp rise in excess deaths after 2010, but that federal policy changes that address the root causes of these excess deaths with evidence-based interventions will help alleviate the current national mortality burden. 

"While new therapeutics such as GLP-1s could make a major dent in cardiometabolic mortality, our findings suggest that other policies should be considered too," says Dr. Bor. "Countries that have the same, or even worse, access to advanced medical technology perform far better on these metrics than the US. We need to identify the policies that other countries have implemented, and think about how we can emulate those policies in the US."

Source:
Journal reference:

Bor, J., et al. Causes of Excess Deaths in the US Compared With Other High-Income Countries. JAMA Network Open. DOI: 10.1001/jamanetworkopen.2026.6147. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2848779

Thursday, October 9, 2025

Dietary cholesterol intake and egg consumption in relation to all-cause and cardiovascular mortality after stroke

 But hasn't dietary cholesterol been proven not to be a CVD risk? Hasn't this horse been beaten to death multiple times?

Why Dietary Cholesterol Does Not Matter (For Most People) 

September 2023

Dietary cholesterol intake and egg consumption in relation to all-cause and cardiovascular mortality after stroke


Abstract

The findings on the associations of dietary cholesterol intake and egg consumption with mortality in the general population remain inconclusive. Our objective was to evaluate all-cause and cardiovascular mortality in relation to dietary cholesterol intake and egg consumption in a cohort of stroke survivors, a particularly vulnerable population. We conducted a prospective cohort analysis of 1367 stroke survivors recruited across the United States between 1999 and 2018. Dietary information was evaluated by a 24-h dietary recall at baseline obtained from NHANES while mortality data were derived from the National Death Index with follow-up through 2019. To investigate the associations of dietary cholesterol intake or egg consumption with all-cause and cardiovascular mortality, Cox proportional hazards and restricted cubic splines models were utilized. After a median follow-up of 79.0 months, the incidence per 1000 person-years was 59.9 (95% confidence interval [CI], 55.2–64.9) for all-cause and 23.3 (95% CI, 20.4–26.5) for cardiovascular mortality. Each 100 mg/1000 kcal/day elevation in cholesterol intake was related to raised risk of all-cause (hazard ratio [HR], 1.16; 95% CI, 1.05–1.27) and cardiovascular mortality (HR, 1.15; 95% CI, 1.00–1.31). A greater risk of all-cause mortality was shown in participants consuming > 1 egg/day (HR, 1.40; 95% CI, 1.06–1.84). The dose-response analysis highlighted the lowest risk of all-cause mortality when egg consumption was around 33.3 g/day. The observed correlations of dietary cholesterol intake or egg consumption with all-cause and cardiovascular mortality were stronger in the subgroups with cardiometabolic diseases (obesity, hypertension, diabetes mellitus, hyperlipidemia) or risk factors for cardiometabolic diseases (advanced age). Among stoke survivors, greater dietary cholesterol connects to an escalated risk of all-cause and cardiovascular mortality in a linear manner. Moderate egg consumption (≤ 1 egg/day) is relatively safe and excessive consumption links to an elevated risk of all-cause mortality.

Wednesday, June 28, 2023

Study reveals that wine consumption has an inverse relationship to cardiovascular mortality

The key line in here is: moderate wine consumption is good for cardiac health.

This is absolutely not possible according to this earlier research: 

Here is what your doctor will use, no thinking required:

Safest level of alcohol consumption is none, worldwide study shows

The latest here:

Study reveals that wine consumption has an inverse relationship to cardiovascular mortality

In a recent study published in the Nutrients Journal, researchers aimed to understand the association between wine consumption and cardiovascular mortality, cardiovascular disease (CVD), and coronary heart disease (CHD).

The researchers performed a systematic review and meta-analysis using longitudinal studies, including cohort and case-control studies retrieved from multiple databases, which they searched from their inception to March 2023.

Study: Association between Wine Consumption with Cardiovascular Disease and Cardiovascular Mortality: A Systematic Review and Meta-Analysis. Image Credit: Alefat/Shutterstock.comStudy: Association between Wine Consumption with Cardiovascular Disease and Cardiovascular Mortality: A Systematic Review and Meta-Analysis. Image Credit: Alefat/Shutterstock.com

Background

Cardiovascular diseases account for a high proportion of deaths on a global scale, with CVD-related deaths surging to nearly 18 million in 2017, in which ischemic heart disease (IHD) caused almost half of the deaths. 

A previous meta-analysis suggested a J-shaped relationship between wine consumption and cardiovascular events and that moderate wine intake promoted better cardiovascular health.

A positive effect of wine on CVDs was first reported in 1979, wherein researchers also asserted that different wine components exert protective effects against pathologies, such as coronary heart diseases, CHD-associated mortality, and cancers, such as oral cancer.

Moreover, studies have suggested that de-alcoholized wines (in the absence of ethanol) are protective against thrombosis as they conserve antioxidant effects.

Light to moderate alcohol consumption positively affects general health; for instance, it acts on high-density lipoprotein cholesterol to prevent atherosclerosis, lowers the incidence of IHD, and helps with the prognosis of people at higher risk of coronary complications leading to myocardial infarction.

Excessive drinking, on the contrary, causes over 200 diseases, which makes it a leading cause of deaths globally, i.e., up to three million deaths annually. High-dose alcohol consumption also increases the risk of suicide, per psychiatrists. 

Alcohol interacts with multiple drugs, altering its metabolism or its own. Decreased alcohol metabolism could lead to increased blood alcohol levels. For example, a component in wine, resveratrol, interacts with certain drugs and modifies their metabolism.

Polyphenols of the non-flavonoid family present in red wine, like tannins, provide multiple cardiovascular health benefits. It is also anti-inflammatory, antioxidant, and antimutagenic. Nonetheless, all cardiologist agrees that light to moderate alcohol consumption has a positive effect on cardiovascular health, whereas excessive alcohol drinking elevates the risk of CHD mortality, cancers, etc. 

Mendelian randomization (MR) approaches analyzed the effects of alcohol consumption on CVDs from a genetic viewpoint and found a much-decreased risk of CHDs in carriers of the alcohol dehydrogenase 1B (ADH1B) gene when they consumed less alcohol.

Likewise, studies have shown a positive effect of wine intake on nonfatal CHD, and beer consumption poses a higher risk of a nonfatal stroke. Based on these observations, researchers have hypothesized that wine components might benefit health. 

Since studies have never stratified these effects by the type of alcohol, perhaps, the researchers assumed that all alcoholic beverages had similar beneficial effects on cardiac health. However, there is a lack of scientific evidence of which alcoholic beverages could be less harmful to CVDs.

About the study

In the present study, researchers explored the association between the incidence of CVD, cardiovascular mortality, and CHD (all cardiovascular events) and wine consumption and attempted to elucidate its nature.

First, they compared the impact of wine on participants who consumed wine against those who did not. Additionally, they analyzed whether the study design characteristics and participant traits like age and smoking affected this association.

This systematic review and meta-analysis included studies with subjects older than 18. The exposure and outcome of included studies were wine consumption and cardiovascular events, respectively. 

The team evaluated the risk of bias in cohort studies using the quality assessment tool devised by the United State's National Heart, Lung, and Blood Institute. They used another similar tool to assess the risk of bias in the case–control studies.

Finally, two independent reviewers graded the cumulative risk of bias for each study - as good, fair, or poor; and found that the overall risk of bias for each included study was 100%. 

In the meta-analysis, they included studies with a greater sample size. They computed the relative risk (RR) and odds ratios (OR) for the correlation between wine consumption and cardiovascular events and converted hazard ratios (HR) reported in some studies to RR.

The team also calculated the pooled RRs for the effect of wine consumption on the risk of CHD, CVD, and cardiovascular mortality using DerSimonian and Lair random effect models. Finally, the team used Egger's test to show publication bias evidence for the association between CVD and wine consumption.

Results

After an extensive search for research studies, the authors retrieved 7,042 articles from nine countries with 1,443,245 subjects and a cumulative follow-up period between four and 25 years. However, the final analytical set for this systematic review and meta-analysis comprised 25 and 22 studies, respectively. In addition, there were four case–control and 21 cohort studies.

Regarding cardiovascular events, seven, 13, and seven studies reported CVD, CHD, and cardiovascular mortality, respectively. Many studies did not report the quantity of wine consumed; thus, researchers could not determine its effect.

The current review and meta-analysis added to the previous evidence of an inverse association between the consumption of wine and three cardiovascular events evaluated in this study.

Importantly, participants' average age, the proportion of women, the follow-up duration, or smoking status did not affect this association. Accordingly, the pooled RRs for CHD, CVD, and cardiovascular mortality were 0.76, 0.83, and 0.73, respectively, all with 95% confidence intervals (CIs). 

Though the observed inverse association applied to red and white wine, the variations in the strength of this association were attributable to the different concentrations of some components. 

Red wine has phenolic compounds, such as gallic acid, catechin, and epicatechin (flavonols), which gives it antioxidant properties. They also reduce low-density lipoprotein (LDL) oxidation, thrombosis risk, plasma, and lipid peroxide.

Also, alcoholic components of wine reduce thrombosis risk and fibrinogen levels and induce collagen and platelet aggregation. Thus, higher consumption of red wine is more beneficial for combating CVDs than other alcoholic beverages.

Conclusions

The current study results confirmed the existing data that moderate wine consumption is good for cardiac health. However, researchers should interpret these findings with caution. Increasing wine consumption could harm patients susceptible to alcohol due to age, preexisting pathologies, or medications.

Based on the findings of this review, wine could be a part of other dietary recommendations. For instance, the Mediterranean diet includes wine and recommends its use for health benefits. However, studies must assess and delineate the effect of wine drinking by the type of wine.

Journal reference:

Friday, November 13, 2020

Chili Pepper Consumption and Cardiovascular Mortality

Well your doctor should have already been prescribing you this particular pepper for delivering  the equivalent of 50 light taps to the brain per second.

Tingling sensation caused by Asian spice could help patients with chronic pain 

September 2013

The latest here:

 Chili Pepper Consumption and Cardiovascular Mortality

Introduction

In this issue of the Journal, a report from an Italian population-based study indicates that intake of hot chili pepper was associated with a significant reduction of all-cause cardiovascular and cerebrovascular mortality (1). In the Moli-sani study, 22,811 men and women were enrolled between 2005 and 2010 and were followed for 8.2 years. During that time, there were 1,236 deaths, 36% of which were cardiovascular, 39% were from cancer, and 25% were from other causes. Chili peppers were consumed >4 times/week by 23.4% of participants, whereas 33.7% of participants never or seldom consumed them. Multivariable risk estimates contrasting those 2 groups gave a hazard ratio (HR) of 0.77 (95% confidence interval [CI]: 0.66 to 0.90) for all-cause mortality, 0.66 (95% CI: 0.50 to 0.86) for cardiovascular disease, 0.56 (95% CI: 0.35 to 0.87) for ischemic heart disease, and 0.39 (95% CI: 0.20 to 0.75) for cerebrovascular death. The effect of chili pepper was independent of a number of factors. In adjusted models, chili pepper consumption was a supplement to the Mediterranean diet score (MDS) and benefit was not seen in hypertensive subjects. It did not appear to be mediated by changes in risk factors such as fasting lipids, glucose, insulin, or other biomarkers. Intake of sweet peppers also reduced mortality risk but to a lesser extent. A small benefit was also observed with intake of vitamin D.

The magnitude of the observed risk reduction was much greater than that in previous studies. In 2015, a Chinese population-based study in ∼500,000 men and women (2) reported that consuming spicy food almost daily was associated with a 14% reduction of total mortality and a 22% reduction of death from ischemic heart disease. In 2017, the U.S. NHANES (National Health and Nutrition Examination Survey) trial reported a 13% risk in total mortality associated with consumption of hot chili peppers (3). Reasons why the magnitude of risk reduction with chili pepper was much greater in the Italian study are not clear, but 1 reason may be that the background diet in Italy was healthier. The U.S. diet was so bad that the American Heart Association statistical report of 2015 indicated that only 0.1% of Americans ate a healthy diet (4). On the basis of that background, it was difficult to show the harm from dietary cholesterol and egg consumption. Early studies showed harm from eggs only among participants who became diabetic (5,6). Only recently did a pooled analysis of data in 29,615 Americans followed for a median of 17.5 years report a dose-dependent increase in cardiovascular risk with both dietary cholesterol and egg consumption (7). Similarly, it may be difficult to show the benefit from any single ingredient in the U.S. diet.

In the Moli-sani study (1), a low MDS (i.e., score of 1 to 3) was observed in 30% of participants, whereas 26% had a high MDS score (score of 6 to 9). Those with a high MDS also had a significant reduction of cardiovascular risk (HR: 0.64; 95% CI: 0.42 to 0.97). The reported HRs were highly adjusted. The full model included adjustment for “age, sex and energy intake, educational level, occupational class, smoking, leisure-time physical activity, cardiovascular disease, cancer, drugs for diabetes, lipid-lowering drugs, medication for hypertension, Mediterranean diet score (deprived of sweet pepper intake), sweet pepper intake (g/day, ordered quartiles), garlic, parsley, and black pepper (consumption yes/no)” (1). Over-adjustment may therefore be a reason for concern. However, risk reduction was observed with regular chili pepper consumption even without adjustment.

Biological plausibility for beneficial effects of chili peppers relates at least in part to obesity and insulin resistance. Chili peppers are the major source of naturally occurring capsaicinoids, including capsaicin, dihydrocapsaicin, nordihydrocapsaicin, homodihydrocapsaicin, and homocapsaicin. Sweet peppers are the major natural source of capsinoids, including capsiate, dihydrocapsiate, and nordihydrocapsiate (8). Capsaicin, the neurotoxin that accounts for the burning sensation of the tongue with chili peppers, reduces diet-induced obesity in rodents and humans and appears to be an activator of AMP-activated kinase and PPAR-γ (9). It increases browning of fat and reduces insulin resistance (10). Capsaicin also appears to have antiplatelet and anticoagulant activity, to reduce low-density lipoprotein oxidation, (8) and to improve endothelial function (11). Figure 1 shows the enormous range of “heat” in varieties of chili peppers.

Figure 1.

A Range of “Heat” in Chili Peppers

There is an enormous range of “heat” in chili peppers, as assessed by the Scoville scale. It is probably not necessary to endure severe neurotoxicity to achieve the cardiovascular benefits of chili peppers.

Should we all begin taking tablets of capsaicin and dousing our food with hot sauce? The history of food supplements suggests that we should wait for randomized trials. A recent meta-analysis of randomized trials of food supplements (vitamins and antioxidants such as vitamins C, D, E, niacin, beta carotene, selenium, and zinc) reported that only folic acid reduced cardiovascular disease and stroke risk and that vitamin B complexes that included vitamin B12 reduced the risk of stroke; no other supplement reduced cardiovascular risk (12). (Reduction of stroke with B vitamins was obscured in early trials by harm from cyanocobalamin among participants with impaired renal function [13].)

What appears to be most beneficial is the eating pattern, rather than any one food. The Mediterranean diet, which is high in whole grains, fruits, vegetables, and legumes, is high in beneficial phytochemicals. Because it is a “mainly vegetarian diet” (14), the Mediterranean diet is also low in cholesterol and saturated fat. As the fat intake is high (40% of calories from fat, mainly olive oil) (15), the diet also has a low glycemic index. In an Israeli diet study, the Mediterranean diet was clearly better than either a low-fat or low-carbohydrate diet for lowering fasting glucose and reducing insulin resistance among diabetic participants (16). In secondary prevention, the Mediterranean diet was twice as effective in the Lyon Diet Heart study (17) as was simvastatin in the contemporaneous Scandinavian Simvastatin Survival Study (18) (a reduction of >60% in coronary risk in 4 years vs. a 40% reduction in 6 years, respectively). In primary prevention, the Mediterranean diet reduced cardiovascular events by 30% over 5 years (19). (Results were confirmed in a re-analysis of the data after excluding participants who were not strictly randomized; persons in the same household were allocated to the same diet after 1 was randomized; and at 1 study site, all participants were allocated to the Mediterranean diet.) Thus, adopting the Cretan Mediterranean diet would be much more likely to reduce cardiovascular risk than adding Tabasco sauce (McIlhenny Co., Avery Island, Louisiana) to the unhealthy American diet.

Footnotes

Dr. Spence is a consultant for Amgen and Orphan Technologies; is an officer of Vascularis Inc.; and has received lecture fees from Pfizer and Bristol-Myers Squibb.