Get Your Cholesterol Even Lower and Start Younger, New Guideline Says

 

Sorry, but cholesterol is not the problem; INFLAMMATION IS! Without inflammation the arteries wouldn't be grabbing cholesterol to pack into plaque. Medical personnel took the shortcut and left the real cause still out there. And solving the correct problem would negate use of statins, Big Pharma will never allow such research to be completed.

Why doesn't your doctor know about this? Your doctor, like mine, will use the excuse that statins reduce inflammation.

Inflammation video explaining it here:

The accent is a bit hard to understand and needs to be rerecorded to a laypersons understanding.

Inflammation In Atherosclerotic Plaque Formation YouTube 

The latest here:

Get Your Cholesterol Even Lower and Start Younger, New Guideline Says

This is the main paragraph for us:

Those with at least a 10 percent risk of having a heart attack or stroke in the next 10 years should get their LDL below 70. Those who have already had a heart attack or stroke, or who have peripheral artery disease, should get their LDL below 55.

Cardiologist impressed by experimental pill that significantly lowers cholesterol

 I guess we are still going down the wrong direction! Cholesterol is not the problem; INFLAMMATION IS! Without inflammation the arteries wouldn't be grabbing cholesterol to pack into plaque. Medical personnel took the shortcut and left the real cause still out there. And solving the correct problem would negate use of statins, Big Pharma will never allow such research to be completed.

Why doesn't your doctor know about this?

Inflammation video explaining it  here:

The accent is a bit hard to understand and needs to be  rerecorded to a laypersons understanding.

Inflammation In Atherosclerotic Plaque Formation YouTube 

The latest here:

Cardiologist impressed by experimental pill that significantly lowers cholesterol

An oral PCSK9 inhibitor from Merck is associated with significant reductions in low-density lipoprotein (LDL) cholesterol, according to new data published in The New England Journal of Medicine.[1] All PCSK9 inhibitors on the market today are injectable—an oral option that does not require needles could make a major impact on patient care. 

“Fewer than half of patients with established atherosclerotic cardiovascular disease currently reach LDL cholesterol goals,” lead author Ann Marie Navar, MD, PhD, an associate professor of cardiology at the University of Texas Southwestern Medical Center in Dallas, said in a statement. “An oral therapy this effective has the potential to dramatically improve our ability to prevent heart attacks and strokes on a population level.”

Back in November, researchers presented initial findings from this study at the American Heart Association’s Scientific Sessions 2025 conference. Now, however, the analysis can be read in full.

The CORALreef Lipids trial focused on nearly 3,000 heart patients with high LDL cholesterol who were randomized to either receive enlicitide, Merck’s experimental oral PCSK9 inhibitor, or a placebo. Two patients received the new drug for every one patient treated with a placebo.

The mean age was 63 years, and the mean LDL cholesterol at baseline was 96.1 mg/dl. All patients were either already on statin therapy or were known to be intolerant to statins. They took their medication—enlicitide or the placebo—daily and were followed for a full year. 

Overall, the study’s primary endpoint—the mean change in LDL cholesterol from baseline to week 24—was -57.1% for the enlicitide group and 3% for the placebo group. The adjusted between-group difference after 24 weeks was -55.8 percentage points.  After the full year, meanwhile, the adjusted between-group difference was -47.2 percentage points. Apolipoprotein B levels and lipoprotein(a) levels were also significantly improved for the enlicitide group compared to the placebo group.

“These reductions in LDL cholesterol are the most we have ever achieved with an oral drug by far since the development of statins,” Navar said.

Another key takeaway from this study was the fact that enlicitide was not linked to any increased risk of adverse safety events. No patients had to stop taking the drug due to safety concerns. Another specific outcome of interest for the group was new-onset/worsening diabetes mellitus. The group found no signs of this being an issue for any individuals randomized to receive enlicitide.

This study, which was funded in full by a subsidiary of Merck, is just the beginning for researchers. Additional research is already underway to specifically examine this pill’s ability to reduce an individual’s risk of myocardial infarction, stroke or other cardiovascular outcomes.

Click here to read the full analysis.

American Heart Association: Use of statins does not pose undue risk of neurological complications

 But you still haven't gotten to the real cause of atherosclerosis, cholesterol is NOT the problem; inflammation is, without inflammation cholesterol won't be grabbed from the bloodstream and packed into plaque.  And solving the correct problem would negate use of statins, Big Pharma will never allow such research to be completed.

Why doesn't your doctor know about this?

Inflammation video explaining it  here:

The accent is a bit hard to understand and needs to be  rerecorded to a laypersons understanding.

Inflammation In Atherosclerotic Plaque Formation YouTube

American Heart Association: Use of statins does not pose undue risk of neurological complications

By Larry Goldstein Monday

Larry Goldstein, M.D., chair of the University of Kentucky’s Department of Neurology, co-director of the Kentucky Neuroscience Institute. Photo provide by UK HealthCare.

The University of Kentucky Public Relations & Strategic Communications Office provides a weekly health column available for use and reprint by news media. This week’s column is by Larry Goldstein, M.D., chair of the University of Kentucky’s Department of Neurology, co-director of the Kentucky Neuroscience Institute and interim medical director of the UK HealthCare/Norton Healthcare – Stroke Care Network.

LEXINGTON, Ky. (June 24, 2024) - Statins, drugs often used in the treatment of patients with or at higher risk of atherosclerotic cardiovascular disease, do not put people at an increased risk of neurological complications, the American Heart Association (AHA) said in a recently issued scientific statement.

A committee I have the privilege of chairing recently wrote the AHA statement, which is connected to a core function of statins: reducing low-density lipoprotein cholesterol (LDL-C). High levels of LDL-C are associated with atherosclerosis, or the thickening and hardening of the arteries. This can lead to heart attack, stroke, blood clots and other complications affecting the cardiovascular system. 

We know that statins and other medications to lower cholesterol levels have a dramatic impact in reducing the risk for cardiovascular disease in general, but cardiac disease and stroke in particular. However, these medications aren’t prescribed as frequently as they could be, in part, because of concern about potential side effects. There isn’t any credible evidence that lipid lowering with statins or other medications increases the risk of developing Alzheimer’s disease or major cognitive impairment which have been public concerns.

Some older studies suggested that statins and the lowering of LDL-C might be associated with cognitive impairment or dementia. According to the AHA, “the preponderance of observational studies and data from randomized trials do not support this conclusion.” Additionally, there is no evidence that the use of statins and other lipid lowering medications worsens the symptoms of patients already diagnosed with Alzheimer’s disease, dementia or other cognitive impairments.

The AHA statement also notes the risk of a hemorrhagic stroke in patients with no cerebrovascular disease is “small and consistently nonsignificant.” A hemorrhagic stroke is caused by the rupture of a blood vessel in or on the brain; they are responsible for about 13 percent of stroke cases.

In primary prevention, folks who haven’t had a stroke or myocardial infarction (heart attack), but are at risk because of high lipid level or other factors, there is virtually no evidence that lowering lipid levels — even to very low levels — increases the risk of brain hemorrhage.

What does this mean?

• Patients who use a statin or other drug to lower LDL-C are not at increased risk of developing Alzheimer’s disease or other major cognitive impairment.
• Patients who use a statin or other drug to lower LDL-C, and have not suffered a stroke or heart attack, are not at increased risk of hemorrhagic stroke.
• Patients living with Alzheimer’s disease or another form of cognitive impairment are not at increased risk of worsening symptoms if they also use a statin or other drug to lower LDC-C.
• There is a significant number of patients who could benefit from statins and other lipid-lowering drugs who do not currently use them.

The benefit in reducing stroke, myocardial infarction and vascular events well outweigh even the small, theoretic risk. The gap between the use of these medications and the potential benefit is pretty wide. There is a large population of patients who could benefit who are not taking advantage of these medications or of this treatment approach. As always, patients should discuss the potential benefits and risks of any treatment with their health care provider.

If you would like to learn more, click here to watch a video about the statement.

UK HealthCare is the hospitals and clinics of the University of Kentucky. But it is so much more. It is more than 10,000 dedicated health care professionals committed to providing advanced subspecialty care for the most critically injured and ill patients from the Commonwealth and beyond. It also is the home of the state’s only National Cancer Institute (NCI)-designated Comprehensive Cancer Center, a Level IV Neonatal Intensive Care Unit that cares for the tiniest and sickest newborns, the region’s only Level 1 trauma center and Kentucky’s top hospital ranked by U.S. News & World Report.

As an academic research institution, we are continuously pursuing the next generation of cures, treatments, protocols and policies. Our discoveries have the potential to change what’s medically possible within our lifetimes. Our educators and thought leaders are transforming the health care landscape as our six health professions colleges teach the next generation of doctors, nurses, pharmacists and other health care professionals, spreading the highest standards of care. UK HealthCare is the power of advanced medicine committed to creating a healthier Kentucky, now and for generations to come. 

Brigham and Women’s Hospital and NCATS Scientists Dial Up an Approach Against Out-of-Control Inflammation

Since resolvins were first identified in 2002  and this from Aug. 2016;

Resolvins, generated naturally from fish oil, show promise as anti-inflammation treatment.  Aug. 2016

Has your stroke doctor and hospital done ONE DAMN THING to initiate further research? Or it is not their responsibility?  You as a patient are responsible for finding and fixing your inflammation problems? Good to know that the stroke medical world has their head in the sand or up their ass doing nothing.  You fix inflammation and statins are no longer needed since cholesterol won't be picked out of the bloodstream and packed into plaque.  Which is why this approach will never see the light of day. Big Pharma will kill it.

Brigham and Women’s Hospital and NCATS Scientists Dial Up an Approach Against Out-of-Control Inflammation

Inflammation is an important part of the immune system’s response to injury and infection. It signals the body to heal and repair damaged tissue and defend itself against invaders such as viruses and bacteria.
Normally, inflammation is temporary; the body has a process to halt it. But when the process breaks down because of an aging immune system, genetic disorder, or other cause, inflammation can become chronic and can contribute to diseases, including some cancers, heart disease, rheumatoid arthritis and neurodegenerative disorders.
Current anti-inflammatory drugs mostly target the chemical trigger that prompts inflammation to begin or increase. But NCATS scientists, working with investigators at Brigham and Women’s Hospital in Boston, are investigating a different strategy to fight inflammation. Instead of attacking what sets it off, they are trying to take advantage of the body’s ability to quiet it down. The scientists have identified compounds that can mimic the activity of chemicals called resolvins, which step up the body’s natural ability to regulate inflammation. The findings, reported in Cell Chemical Biology (link is external), open the door to a potential new approach to treat out-of-control inflammation.
Resolvins reduce inflammation by reducing the activity of immune system cells that are called into action by infection or injury. Scientists think that mimicking the effects of resolvins might be useful in treating excessive inflammation and the diseases it can cause. But producing compounds that can mimic these effects has been difficult. Resolvins have complicated, unstable chemical structures and are short-lived; they exist only to shut down inflammation, and then they disappear.
About six years ago, NCATS scientists Marc Ferrer, Ph.D., Noel Southall, Ph.D., and Juan Marugan, Ph.D., began collaborating with Charles Serhan, Ph.D., D.Sc., director of the Center for Experimental Therapeutics and Reperfusion Injury at Brigham and Women’s Hospital. Serhan was studying resolvins and similar substances that had comparable effects to reduce inflammation. Serhan and colleagues first discovered resolvins in 2002. Since then, his lab has advanced much of the understanding of the way resolvins work on immune cells through chemical docking stations called receptors. This interaction sends out a flood of chemical signals telling the immune system to stand down and naturally reduce inflammation.

Human resolvin receptor shown with several attached molecules represented in green, blue, red, cyan, violet and magenta. Each can potentially turn on anti-inflammatory activity.

Serhan found that a type of resolvin called resolvin D1 reduced inflammation in the nervous system and worked through a protein, GPR32, which is a receptor type called a G protein-coupled receptor. Other types of resolvins work through different receptors. Harnessing the body’s ability to control neurological inflammation could help treat spinal injury, stroke and Alzheimer’s disease.
“It’s very appealing,” said Ferrer. “For neurological disorders, such as spinal injury or stroke, inflammation makes the neurological damage worse. We want to explore how controlling its resolution can help with disease treatment.
At the same time, a better understanding of resolvins was needed.
Serhan approached NCATS for help finding other molecules that were more stable than resolvins but could carry out the same function. Ferrer, Southall, Marugan and their NCATS colleagues used a technique called high-throughput screening to sort through more than 48,000 candidate compounds at the same time. The screening used a series of tests to look for molecules that could activate human GPR32.
The team identified four compounds that had the most potential to turn on the body’s mechanism to reduce inflammation. Two are known molecules, and the other two have novel chemical structures. Serhan and his colleagues confirmed the anti-inflammatory and inflammation-resolving activity of the compounds in separate tests.
“It’s the first time anyone has had synthetic molecules that could potentially modulate this receptor,” Marugan said, adding that the findings have helped explain the effects of resolvins and similar molecules. “This provides an opportunity to develop a new kind of drug to reduce inflammation.”
According to Marugan, the work established an approach that researchers can use to discover and develop better candidate drugs more efficiently. At the same time, studying molecules that can reduce inflammation allows NCATS scientists to gain a better understanding of the intricate relationship between inflammation and the immune system.
“The next step would be for medicinal chemists to further optimize and make these four molecules more specific, potent and drug-like,” Marugan said. “These molecules are starting points for drugs, and further testing will be needed.”
The Brigham-NCATS group would still like to better understand the molecular bases of how GPR32 interacts with resolvins and other chemicals and how this interaction affects the chemical cues sent to immune cells to halt inflammation.
Posted March 2019

Study examines the rise of plaque in arteries

Maybe we could finally address the root cause of atherosclerosis rather than taking statins to lower cholesterol levels. But statins are a cash cow for Big Pharma, they won't go lightly even with overwhelming evidence.  Probably won't occur in my lifetime. 

Study examines the rise of plaque in arteries

The accumulation of cholesterol plaques in artery walls can lead to atherosclerosis, or the hardening of arteries that contributes to heart attacks and strokes. In a new study, Yale researchers investigate how plaque cells develop at the molecular level, and their findings could help produce targeted treatments for the disease.

Smooth muscle cells, the dominant type of cell found in artery walls, are known to be involved in plaque build-up, but it has not been clear how this occurs. The research team, led by senior study author Daniel Greif, used mice models and primary human cells to study smooth muscle cells and their contribution to atherosclerotic plaques.

They discovered that a single smooth muscle cell gives rise, through a process of clonal expansion, to the majority of cells found in the plaque. Additionally, they learned that a gene known as integrin beta3 regulates the migration of a single smooth muscle cell progenitor from the artery wall into plaque. Once inside the plaque, the progenitor cell reproduces and changes into other cell types. Further, the researchers determined that the gene's role in plaque development occurs in smooth muscle cells as well as in bone marrow-derived cells.   

Together, the findings shed light on the complex mechanisms behind the progression of atherosclerosis, and suggests potential targets for future therapies, the researchers note.

The study is published in Nature Communications.

Effect of Probiotics on Blood Pressure

Nothing will occur about your doctor prescribing food for blood pressure reduction, Big Pharma is in charge. You can't do this on your own, that would be dangerous with your doctor not knowing about it. Followup is needed to have amounts needed per body weight.Or maybe you want to talk to your doctor about this:

Beet Juice Beats Hypertension April 2013

Except for this possible problem;

Beet juice can lower blood pressure — sometimes too much April 2017

The latest here:

Effect of Probiotics on Blood Pressure

A Systematic Review and Meta-Analysis of Randomized, Controlled Trials

Saman Khalesi, Jing Sun, Nicholas Buys, Rohan Jayasinghe

Download PDF

https://doi.org/10.1161/HYPERTENSIONAHA.114.03469

Hypertension. 2014;64:897-903

Originally published July 21, 2014

Abstract

Previous human clinical trials have shown that probiotic consumption may improve blood pressure (BP) control. The aim of the present systematic review was to clarify the effects of probiotics on BP using a meta-analysis of randomized, controlled trials. PubMed, Scopus, Cochrane Library (Central), Physiotherapy Evidence Database, and Clinicaltrial.gov databases were searched until January 2014 to identify eligible articles. Meta-analysis using a random-effects model was chosen to analyze the impact of combined trials. Nine trials were included. Probiotic consumption significantly changed systolic BP by −3.56 mm Hg (95% confidence interval, −6.46 to −0.66) and diastolic BP by −2.38 mm Hg (95% confidence interval, −2.38 to −0.93) compared with control groups. A greater reduction was found with multiple as compared with single species of probiotics, for both systolic and diastolic BP. Subgroup analysis of trials with baseline BP ≥130/85 mm Hg compared with <130/85 mm Hg found a more significant improvement in diastolic BP. Duration of intervention <8 weeks did not result in a significant reduction in systolic or diastolic BP. Furthermore, subgroup analysis of trials with daily dose of probiotics <10¹¹ colony-forming units did not result in a significant meta-analysis effect. The present meta-analysis suggests that consuming probiotics may improve BP by a modest degree, with a potentially greater effect when baseline BP is elevated, multiple species of probiotics are consumed, the duration of intervention is ≥8 weeks, or daily consumption dose is ≥10¹¹ colony-forming units.

More at link.

Analysis: No Statin Primary Prevention Seen for Seniors

Since you had a stroke you don't fall into this primary prevention category. Notice all the 'experts' pooh-poohing this analysis. You wouldn't want to reduce the profits of Big Pharma.
https://www.medpagetoday.com/Cardiology/Atherosclerosis/65492?

Post hoc analysis turns up no benefit at ages 65-74

• by Crystal Phend
  Senior Associate Editor, MedPage Today May 23, 2017

Seniors don't get a cardiovascular or mortality benefit from taking a moderate-dose statin for primary prevention, according to a post hoc subgroup analysis of ALLHAT-LLT.
In the overall neutral open-label trial, analysis restricted to participants ages 65 and older, showed that randomization to pravastatin (Pravachol) likewise didn't impact the primary endpoint of all-cause mortality during 6 years, Benjamin Han, MD, MPH, of the New York University School of Medicine in New York City, and colleagues reported online in JAMA Internal Medicine.
In the 65- to 74-year-olds, the mortality rate was 15.5% on pravastatin and 14.2% with usual care (HR 1.08, P=0.55). For adults 75 years and older, the trend actually neared significance in the wrong direction (24.5% pravastatin vs 18.5%, HR 1.34, P=0.07).
Coronary heart disease events came out similar between groups, including after multivariable regression, with no treatment by age interaction.
The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial-Lipid-Lowering Trial -- nested within the ALLHAT hypertension trial -- included 2,867 ambulatory adults, ages 65 and older, for the analysis out of the overall population 55 and older with hypertension and at least one additional heart disease risk factor. No one had baseline atherosclerotic cardiovascular disease (ASCVD) or baseline statin use.
An accompanying editor's note by Gregory Curfman, MD, of Harvard Medical School in Boston, acknowledged statin risks that "may be particularly problematic in older people" and concluded the ALLHAT-LLT results "should be considered before prescribing or continuing statins for patients in this age category."
Physicians contacted by MedPage Today were universally skeptical that the analysis should have any clinical impact.
"I think the most important part of this report may be the section on Limitations, which states that it is a post hoc secondary analysis of a trial of a subgroup of patients. I always tell students to avoid this type of analysis," commented Daniel Blumenthal, MD, MPH, president of the American College of Preventive Medicine.
James Stein, MD, director of the Preventive Cardiology Program at the University of Wisconsin in Madison, pointed to the "null bias due to the small difference in achieved LDL-C" between groups.
While agreeing that post hoc subgroup analyses can be misleading, Noel Bairey-Merz, MD, director of the Preventive Cardiac Center at Cedars-Sinai Medical Center in Los Angeles, noted that "given the declining CVD mortality rate in the U.S., particularly in the over 65-year-olds, due to improved public health (less smoking) and healthcare (Medicare), demonstration of mortality benefit of anything now is rare."
Kim Williams, MD, of Rush University in Chicago and a past president of the American College of Cardiology, pointed to the moderate 40-mg pravastatin dose used, too. While the findings might seem to contradict the ACC/American Heart Association lipid guidelines, he noted that the study was consistent with a 15% to 30% relative reduction in coronary events, although not significant.
"This suggests a type II statistical error (accepting the null hypothesis when it is actually false) and that a larger study would have been positive," he told MedPage Today by email.
Chris Cannon, MD, of Brigham and Women's Hospital who has been involved in key lipid trials, noted that about one-third of the usual care group ended up on statins. In contrast to the modest sample size and lack of placebo control of the ALLHAT-LLT analysis, he pointed to pooled data meta-analysis from the HOPE-3 and JUPITER double-blind, placebo-controlled primary prevention trials with five times more seniors.
"It shows clear benefit," he said. "Which would you believe?"
One of the authors of that analysis, Paul Ridker, MD, also of Brigham and Women's Hospital, noted no heterogeneity across age groups in that analysis -- under 65, 65 to 69, and 70 or older.
"Of course, when our paper came out last month, there was no media coverage and we did not issue a press release because we did not think a paper confirming what is already known was particularly newsworthy," he said in an email to MedPage Today.
The study shouldn't undermine the value of statins for older adults, Stein suggested.
"Statins clearly reduce risk of myocardial infarction and stroke among older adults without established ASCVD," he added. "I treat a lot of older patients and the vast majority would be very pleased to avoid a heart attack or stroke, even if it's not clear if they will live longer. Many studies have addressed this issue and are included in a meta-analysis from 2013, which included ALLHAT-LLT. There are subgroup analyses of large statin trials showing similar results.
"An open question is at what age should we stop screening and treating lipids for primary prevention. It's not known, though epidemiological data suggest it may be around 85 years of age. Medical care and decision-making always should be a shared interaction with patients, but especially very old patients who may have competing risks, polypharmacy, and limited lifespan," Stein stated.
An Australian trial, STAREE, comparing statins versus placebo in people over age 70 is underway, with results expected in 2020.

The study was supported by the National Heart, Lung, and Blood Institute.
Han and co-authors and Curfman disclosed no relevant relationships with industry.

• Primary Source

  JAMA Internal Medicine

  Source Reference: Han BH, et al "Effect of statin treatment vs usual care on primary cardiovascular prevention among older adults: The ALLHAT-LLT Randomized Clinical Trial" JAMA Intern Med 2017; DOI: 10.1001/jamainternmed.2017.1442

• Secondary Source

  JAMA Internal Medicine

  Source Reference: Curfman G "Risks of statin therapy in older adults" JAMA Intern Med 2017; DOI: 10.1001/jamainternmed.2017.1457.

Pot Use Tied to Higher Odds for Stroke, Heart Failure

That is quite a jump from concluding that pot use as specified in the question is tied to heart attacks and stroke.  I tried marijuana in college and nothing about my use of it then led in any way to my stroke. I also drank lots of beer in college and that could just as easily be pointed to as a risk factor for stroke and heart attack.  False association but good for big pharma to demonize marijuana. I will try it for rehab after my next stroke. This is total biased research, they had an agenda to write on and they manufactured the conclusions.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.

http://www.philly.com/philly/health/topics/HealthDay720422_20170309_Pot_Use_Tied_to_Higher_Odds_for_Stroke__Heart_Failure.html
New research analyzing millions of U.S. medical records suggests that marijuana use raises an adult's risk of stroke and heart failure.

The study couldn't prove cause-and-effect, but the researchers said they tried to account for other heart risk factors.
"Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients," explained lead researcher Dr. Aditi Kalla, a cardiologist at Einstein Medical Center in Philadelphia.
"That leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects," Kalla said in a news release from the American College of Cardiology (ACC).

Her team is slated to present its findings March 18 at the ACC's annual meeting, in Washington, D.C.
In the study, Kalla's group looked at 20 million health records of patients aged 18 to 55 who were discharged from one of more than a thousand hospitals across the United States in 2009 and 2010.
Of those patients, 1.5 percent said they'd used marijuana.
Such use was associated with a much higher risk for stroke, heart failure, coronary artery disease and sudden cardiac death. Pot use was also tied to common heart disease risk factors such as obesity, high blood pressure, smoking and drinking, the researchers said.

After adjusting for those risk factors, the researchers concluded that marijuana use was independently associated with a 26 percent increased risk of stroke and a 10 percent increased risk of heart failure.
"More research will be needed to understand the [reasons] behind this effect," Kalla said.
Not everyone agreed the findings are cause for alarm, however.
Paul Armentaro is deputy director of NORML, a marijuana advocacy group. He called the increase in heart risk, "a relatively nominal one," and said the study "is inconsistent with the findings of several other longitudinal studies finding that those who consume cannabis, but not tobacco, suffer no greater likelihood of adverse events compared to those with no history of use."
NORML agrees that certain groups -- adolescents, pregnant or nursing mothers, people with a history of psychiatric illness, or those with a prior history of heart disease -- may want to avoid marijuana due to the potential effects on health.
But others may want to talk the issue over with their doctors. "As with any medication, patients should consult thoroughly with their physician before deciding whether the medical use of cannabis is safe and appropriate," Armentaro said. (What the hell good would that do, your doctor knows nothing about benefits of marijuana?)
Study author Kalla noted that medical or recreational marijuana use is now legal in more than half of U.S. states -- so a better understanding of its health effects is needed.
"Like all other drugs, whether they're prescribed or not prescribed, we want to know the effects and side effects of this drug," Kalla said. "It's important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis."
Two heart specialists agreed.
The new study "suggests that marijuana may not be as safe as proponents for its legalization claim,"(bullshit! the study does no such thing) said Dr. Andrew Rogove, who directs stroke care at Southside Hospital in Bay Shore, N.Y. He believes that "further studies need to be performed to elucidate how marijuana use can increase risk for stroke and heart failure and if any particular way that it is used confers a higher risk."
Dr. Shazia Alam directs inpatient stroke services at Winthrop-University Hospital, in Mineola, N.Y. She believes there's a growing number of patients of all ages with a history of marijuana use.
"As more of our patients will be on marijuana in the near future given the legalization trend, this study reminds us how important it is to ask about marijuana use early on and inform them of any potential consequences," she said.

"Moreover, we have been seeing increased strokes in the younger population, therefore routinely inquiring about marijuana use may become an integral part in stroke prevention," Alam added.
Because these findings are to be presented at a medical meeting, they should be considered preliminary until published in a peer-reviewed journal.
More information
The U.S. National Institute on Drug Abuse has more about marijuana. (This proves the bias.)
-- Robert Preidt SOURCES: Shazia Alam, D.O., director, inpatient neurology and stroke services, Winthrop-University Hospital, Mineola, NY; Andrew Rogove, M.D., medical director, stroke, Southside Hospital, Bay Shore, N.Y.; Paul Armentaro, deputy director, NORML; American College of Cardiology, news release, March 9, 2017

Raising ‘good’ cholesterol doesn’t protect against heart disease after all, study finds

All because nobody went after the real cause of atherosclerosis, inflammation, cholesterol is just a side player in this. I wonder if anyone involved here even understands cause and effect. Don't discontinue your statins just because big pharma is making great profits selling drugs for the wrong cause.
How plaque forms: Bet your doctor doesn't explain this.
Inflammation In Atherosclerotic Plaque Formation  
 

New model of arterial thrombus formation is similar to popular video game
Maybe you want this to fix it.
Like maybe this plaque sander?

Analysis: Plaque 'Sander' Safety Durable

Raising ‘good’ cholesterol doesn’t protect against heart disease after all, study finds

“Good” cholesterol might be in for a name change.

Raising HDL, widely known as good cholesterol, for years has been thought to protect against heart attack and stroke. But a big new study published Monday found little evidence it does.

The finding upends the advice doctors have been giving millions of patients — and helps explain why the drug industry has failed time and again, despite billions in investment, to develop a drug that cuts deaths from heart disease by boosting HDL levels.

“When you explain [cholesterol levels] to patients, it’s very easy to say one number’s bad and the other number’s good,” said Dr. Dennis Ko, a cardiologist at Canada’s Institute for Clinical Evaluative Sciences and lead author of the study. But it turns out that HDL is associated with poor health generally and does not seem to affect cardiovascular risk.

In the study, Ko and his colleagues looked at years of data from about 630,000 people in Ontario, sorting their HDL scores from low to high. Those with basement-level HDL were more likely to die of cardiovascular complications, but the risk did not drop steadily as good cholesterol levels rose.

Instead, it dipped, then hit a plateau; people with HDL of about 40mg/dL had roughly the same risk as those with about 80 mg/dL. And death risks actually increased for those with extremely high levels of good cholesterol.
Further muddying the picture, people in the low-HDL group were also more likely to die of diseases unrelated to the heart. And they had lower incomes, higher body weights, and poorer diets than others in the study, all of which correlate with increased mortality on their own.
HDL has been thought to lower cardiovascular risk by cleansing the bloodstream of “bad” cholesterol and scrubbing the inner walls of blood vessels, so your levels of HDL were thought to predict your risk of heart attack or stroke. But this new data suggests HDL may just be a fatty substance along for the ride.
“It may be therefore that it’s reflecting other health habits that lead to greater risk, rather than actually being a risk factor itself,” said Dr. Steven Nissen, a Cleveland Clinic cardiologist not involved in the study.
The study, published in the Journal of the American College of Cardiology, will sound familiar to the drug industry, which has repeatedly failed to design a pill that might improve patients’ lives by increasing HDL.
A decade ago, Pfizer spent more than $800 million to get the HDL-boosting medication torcetrapib into late-stage trials, only to find that more patients died on the drug than on placebo. Roche was next to fail when its drug, dalcetrapib, came up short in a 16,000-patient trial in 2012. And last year, Eli Lilly shut down a study testing its evacetrapib on 12,000 patients after discovering that the drug had no effect on heart attack and stroke.
Those drugs, called CETP inhibitors, are meant to interrupt the process that turns HDL into LDL cholesterol, its “bad” relative. And, in a sense, they work — Lilly’s pill boosted HDL by about 130 percent and slashed LDL by more than one-third. But, time after time, changing that ratio of good to bad cholesterol has failed to improve outcomes for patients.

Despite the litany of disappointments, there’s one CETP pill still in the ring. Merck is in the final phase of a 30,000-patient study on anacetrapib, the last of the class in late-stage development. Results are expected early next year, but optimism does not abound.
“I have very little hope that the ongoing trial is going to work,” said Nissen, who chaired Lilly’s failed evacetrapib study. “And if you think about it, if that study also fails, what is the likelihood that anybody will do another large, Phase 3 trial? I think the answer is probably pretty low.”
Still, cardiologists said it may still be useful to keep measuring HDL in blood lipid tests, because it does seem to be correlated with other factors that can affect health, such as diet and exercise habits. Doctors can gather such information with questionnaires, but those are time-consuming and rely on patients accurately recounting their habits.
And HDL may yet redeem itself in the world of drug development. Good cholesterol is complex, with various particle sizes and subspecies floating around in the body. Ko and his colleagues applied a broad brush in their study, looking at HDL as a monolith. It’s possible a deeper look at HDL subtypes could reveal a more nuanced relationship with cardiovascular disease, Dr. Stephen Nicholls and Dr. Peter Psaltis wrote in an editorial accompanying the study.
And it’s possible that drugs to raise HDL may work only in people with certain genetic mutations.

Read More

New dietary guidelines tougher on meat, easier on cholesterol

Last year, mining the wreckage of Roche’s failed dalcetrapib study, researchers at the University of Montreal noted that the drug had a marked effect on a subset of patients with mutations to a gene called ADCY9. DalCor Pharmaceuticals, a UK startup, has raised $150 million in venture capital to see if Roche’s drug can have a second life as a targeted therapy.
“Our understanding of the HDL story has changed,” said Dr. Bassem Masri, a cardiovascular disease expert at Weill Cornell Medicine and NewYork-Presbyterian who helped run a slew of CETP trials. “It’s not just [about] increasing HDL; it might be that only a specific population will respond to that increase positively.”
Elsewhere, scientists are studying novel methods of boosting HDL, whether by stimulating other pathways in the body or injecting patients with synthetic good cholesterol. Considering past failures, it looks like an uphill battle. But anything’s possible.
“I’ve been doing medicine long enough that I’ve learned to say you never say never,” Nissen said.

Pharma CEO: We’re in Business of Shareholder Profit, Not Helping the Sick

Don't ever expect companies like this to find drugs to help stroke survivors. Finding and approving a drug is way too expensive with an uncertain chance of working. This is precisely why we need a great stroke association running clinical trials and creating drugs, getting the money from foundations who want to be associated with successful interventions that help reduce the impact of stroke. This is a no-brainer but with never occur with the fucking failures of stroke associations we have today.
http://usuncut.com/class-war/valeant-ceo-shareholder-profit/
Last month, Martin Shkreli became a household name. The CEO of Turing Pharmaceuticals is now infamous for raising the price of a newly-acquired drug to $750 a pill. He also explained in an interview that his company was not alone in acquiring drugs currently on the market to raise their price and, in turn, rapidly drive up their stock price.
Enter J. Michael Pearson,  The current CEO of Valeant Pharmaceuticals who recently said that his company’s responsibility is to its shareholders, while making no mention of his customers who rely on his drugs to live.

“If products are sort of mispriced and there’s an opportunity, we will act appropriately in terms of doing what I assume our shareholders would like us to do.”

Already this year, Valeant has increased the price of 56 of the drugs in its portfolio an average of 66 percent, highlighted by their recent acquisition, Zegerid, which they promptly raised 550 percent. Not only does this have the unfortunate side effect of placing the price of life-saving drugs out of reach for even moderately-insured people, but it has now begun to call into question the sustainability of this rapidly-spreading business model.
In an interview with CNBC, Pearson defended his business practice of acquiring drugs instead of investing in research and development.

“My primary responsibility is to Valeant shareholders. We can do anything we want to do. We will continue to make acquisitions, we will continue to move forward.”

Since being named CEO in 2008, Valeant has acquired more than 100 drugs and seen their stock price rise more than 1,000 percent with Pearson at the helm. But it appears that all of the public backlash over price gouging of prescription drugs, which has included both Hillary Clinton and Bernie Sanders taking a stance against the practice as a platform in their respective presidential campaigns, has placed the practice under tremendous scrutiny.
The House Committee on Oversight and Government Reform is planning to issue a subpoena for information on recent price increases from both Pearson and Shkreli.
And that pending investigation has sent Valeant’s stock price tumbling more than 27 percent in the last month, which may have shareholders concerned enough to wonder if Pearson pushed too hard for too long.

Adverse effects of cannabis scientifically verified

The title is alarmist, didn't see the alarm in the writeup itself. I'm sure only negative results are going to posted for a while since marijuana could replace a lot of drugs and ruin big pharma profits. So rather than focus on the 'have potential' statement you get the alarmist, 'causes disruption' 'may be harmful'
http://medicalxpress.com/news/2016-09-adverse-effects-cannabis-scientifically.html
Researchers have clarified important mechanisms involved in the formation of neural circuits in the brain. This group also discovered that delta-9-tetrahydrocannabinol (THC), a psychoactive substance also found in cannabis, causes disruption of neural circuits within the cortex. These results explain why cannabis may be harmful and have potential to find application in the functional recovery of brain injury and in cases of dementia.

Neural activity is known to play an important role in the formation of neural circuits. However, we still do not know much about what kind of neural activities are involved in this formation process. This process is especially complex in projections from the thalamus to the cortex, of which so far we only knew that as these projections develop, unnecessary projections are eliminated, thereby leaving only correct projections. A group of researchers led by Fumitaka Kimura, associate professor at the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, has now clarified the involvement of several mechanisms in the formation of this neural circuit. The researchers also put forth scientific evidence that cannabis intake causes the unnecessary trimming of neural connections, leading to a breakdown of neural circuits (Figure 1).
In their study, this group of researchers discovered that in a different section of the cortex, the rule (Spike Timing-Dependent Plasticity: STDP) by which synaptic strength (a functional measure of connections) between neurons was determined suddenly changed at a certain point in development. Building on this finding, the group examined whether a similar STDP change occurred in the projection from the thalamus and the cortex as well. They found that initially, the synapses were strengthened due to the synchronized activities of the pre- (thalamic) and post- (cortical) synaptic neurons. But after the projections had spread widely, the synchronized activities weakened all but some synapses, thereby eliminating unnecessary projections to enable more systematic ones. As the synapses are weakened, endogenous cannabinoid is released from neural cells via these synchronized activities, leading to a regression of unnecessary neuron projections (Figure 2). The researchers also confirmed such regression when cannabinoid was taken in externally.

Endogenous cannabinoid regulates the termination area of thalamocortical axons.(left): Normal thalamocortical projection terminates within a square area in layer 4 (barrel, indicated in red), revealed by visualization of individual …more

These findings may have an impact on further research focused on advancing our understanding of the mechanisms involved in the formation of neural circuits and have the potential to lead to the development of new therapies to improve recovery from brain damage and dementia. In addition, the findings provide scientific evidence for the adverse effects of cannabis consumption on brain development and therefore may help to decrease abuse of marijuana.
This research was featured in the electronic version of Journal of Neuroscience on June 29, 2016.

Explore further: Scientists identify gene that triggers neural remodeling during C. elegans development

More information: C. Itami et al, Developmental Switch in Spike Timing-Dependent Plasticity and Cannabinoid-Dependent Reorganization of the Thalamocortical Projection in the Barrel Cortex, Journal of Neuroscience (2016). DOI: 10.1523/JNEUROSCI.4280-15.2016

Journal reference: Journal of Neuroscience

Cost of new cholesterol drugs unsustainable, says study

This would actually be a very good thing. Cholesterol is not the problem in cardiovascular disease, inflammation is the problem. With no inflammation cholesterol would not be pulled out of the bloodstream and packed into plaque. But I doubt Big Pharma will so easily be defeated. We have no stroke leaders that can set a proper strategy and follow it through to completion. 

Cost of new cholesterol drugs unsustainable, says study

UCSF News

Wide use of PCSK9 inhibitors would increase us drug spending by nearly 40 percent.
A new UC San Francisco–led study using computer models of cardiovascular disease in American adults concludes that the price of a promising new class of cholesterol–lowering drugs called PCSK9 inhibitors would need to be reduced by up to 70 percent to be cost–effective in the United States using commonly accepted standards. “If all eligible US adults were put on PCSK9 inhibitors we’d face an unsustainable increase in healthcare spending,” said Dhruv Kazi, MD, assistant professor of medicine and lead author of the new study, published online in the Aug. 16 issue of JAMA: The Journal of the American Medical Association. First approved by the US Food and Drug Administration in 2015, PCSK9 inhibitors such as alirocumab (Praluent) and evolocumab (Repatha), dramatically reduce levels of so–called “bad,” low–density lipoprotein (LDL) cholesterol – in clinical trials, levels of LDL were reduced by as much as 60 percent in patients taking these drugs. But these drugs have downsides: they must be injected every two to four weeks, and have an annual cost of roughly $14,000 per patient. The model employed in the new UCSF research suggests that prescribing PCSK9 inhibitors to all eligible adults would increase US drug spending by 38 percent, which would represent a 4 percent increase in overall healthcare spending, even after accounting for cost savings from prevented cardiovascular events. To determine the cost–effectiveness of the new drugs, researchers used the Cardiovascular Disease Policy Model, collaboratively developed by UCSF and other institutions, to simulate the cardiovascular health of all U.S. adults by drawing on demographic and health data from public records and other sources. In this study, treatment costs were evaluated for two high–risk populations: those with a family history of high cholesterol and individuals with preexisting cardiovascular disease. The model determined how much it would cost to gain one year of life (known as a “life–year”), adjusted for health status, under three different scenarios. In the first scenario, representing the status quo, only statins were prescribed; a second scenario included PCSK9 inhibitors where appropriate; and a final scenario involved a third cholesterol–lowering drug, ezetimibe (Zetia), which lowers levels of blood LDL by blocking its absorption in the small intestine. While there is no nationally mandated cost threshold for drug treatments, consensus in the medical community suggests that treatments should cost roughly $100,000 per life–year gained or less, Kazi said. The PCSK9 inhibitor scenario of the model estimated it would cost $423,000 to gain one quality–adjusted life–year – well over the accepted threshold. “PCSK9 inhibitors are not cost–effective at present. They would need to come down about 70 percent to meet that mark,” Kazi said. The researchers point out that the model–suggested target price, just over $4,500, is much closer to the cost of PCSK9 inhibitors in Europe, where drug price negotiations with pharmaceutical companies are more common. According to the model, ezetimibe treatment comes in just above the threshold, at $155,000 per quality–adjusted life–year gained. The model also shows, however, that considerable healthcare savings could be realized if statins were more consistently prescribed for patients who could benefit from them. Not all patients who should take statins currently do, for reasons ranging from inadequate medical follow–up to poor health literacy. According to the model, prescribing statins, which cost around $810 annually, for these patients would prevent more than 200,000 major cardiovascular events, bringing savings of $12 billion over five years.