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The human brain is the most complex organ in our body, and is characterized by a unique ability called neuroplasticity. Neuroplasticity refers to our brain’s ability to change and adapt in its structural and functional levels in response to experience. Neuroplasticity makes it possible for us to learn new languages, solve complex mathematical problems, acquire technical skills, and perform challenging athletic skills, which are all positive and advantageous for us. However, neuroplasticity is not beneficial if we develop non-advantageous learned behaviors. One example of non-advantageous learning is habitual drug misuse that can lead to addiction.
Our first decision to use a drug may be triggered by curiosity, circumstances, personality, and stressful life events. This first drug exposure increases the release of a molecule (neurotransmitter) called dopamine, which conveys the feeling of reward. The increased changes in dopamine levels in the brain reward system can lead to further neuroplasticity following repeated exposure to drugs of abuse; these neuroplasticity changes are also fundamental characteristics of learning. Experience-dependent learning, including repeated drug use, might increase or decrease the transmission of signals between neurons. Neuroplasticity in the brain’s reward system following repeated drug use leads to more habitual and (in vulnerable people) more compulsive drug use, where people ignore the negative consequences. Thus, repeated exposure to drugs of abuse creates experience-dependent learning and related brain changes, which can lead to maladaptive patterns of drug use.
A recent learning model proposed by Dr. Marc Lewis in New England Journal of Medicine highlights the evidence of brain changes in drug addiction, and explains those changes as normal, habitual learning without referring to pathology or disease. This learning model accepts that drug addiction is disadvantageous, but believes it is a natural and context-sensitive response to challenging environmental circumstances. Dr. Nora Volkow, director of the National Institute on Drug Abuse (NIDA), and many addiction researchers and clinicians, view addiction as a brain disease triggered by many genetic, environmental, and social factors. NIDA uses the term “addiction” to describe the most severe and chronic form of substance use disorder that is characterized by changes in the brain’s reward, stress, and self-control systems. Importantly, both learning and brain disease models accept that addiction is treatable, as our brain is plastic.
Our brain’s plastic nature suggests that we can change our behaviors throughout our lives by learning new skills and habits. Learning models support that overcoming addiction can be facilitated by adopting new cognitive modifications. Learning models suggest pursing counseling or psychotherapy, including approaches such as cognitive behavioral therapy (CBT), which can help a person modify their habits. NIDA suggests that, for some people, medications (also called medication-assisted treatment or MAT) can help people manage symptoms to a level that helps them pursue recovery via strategies such as counseling and behavioral therapies, including CBT. Many people use a combination approach of medications, behavioral therapies, and support groups to maintain recovery from addition.
CBT is an example of a learning-based therapeutic intervention; thus, it utilizes neuroplasticity. Scientific evidence suggests that CBT, alone or in combination with other treatment strategies, can be effective intervention for substance use disorders. CBT teaches a person to recognize, avoid, and learn to handle situations when they would be likely to use drugs. Another example of evidence-based behavioral therapy that has been shown to be effective for substance use disorders is contingency management. Contingency management provides a reward (such as vouchers redeemable for goods or movie passes) to individuals undergoing addiction treatment, to reinforce positive behaviors such as abstinence. This approach is based on operant conditioning theory, a form of learning, where a behavior that is positively reinforced tends to be repeated. Overall, multiple evidence-based approaches are used for the treatment of substance use disorders that require learning and utilize neuroplasticity.
Our brain is plastic, and this trait helps us learn new skills and retrain our brain. As the brain can change in a negative way as observed in drug addiction, the brain can also change in a positive way when we adopt skills learned in therapy and form new, healthier habits.
Targeting Behavioral Therapies to Enhance Naltrexone Treatment of Opioid Dependence: Efficacy of Contingency Management and Significant Other Involvement. Archives of General Psychiatry, August 2001.
Efficacy of Disulfiram and Cognitive Behavior Therapy in Cocaine-Dependent Outpatients: A Randomized Placebo-Controlled Trial. Archives of General Psychiatry, March 2004.
Cognitive Behavioral Therapy and the Nicotine Transdermal Patch for Dual Nicotine and Cannabis Dependence: A Pilot Study. American Journal on Addictions, May-June 2013.
Brain Change in Addiction as Learning, Not Disease. New England Journal of Medicine, October 18, 2018.
Cognitive Behavioral Therapy for Substance Use Disorders. The Psychiatric Clinics of North America, September 2010.
Neurobiologic Advances from the Brain Disease Model of Addiction. New England Journal of Medicine, January 28, 2016.
The post Brain plasticity in drug addiction: Burden and benefit appeared first on Harvard Health Blog.
As lockdowns have kept people at home and out of medical facilities, infant vaccination rates have dropped. As you might expect, this is bad news for the drug industry, which is likely why they’ve started promoting baseless claims that childhood vaccinations might prevent COVID-19 deaths.
There’s absolutely no evidence for this, yet, in March 2020, they started pushing the TB vaccine, claiming it might “steel the immune system” against SARS-CoV-2. As reported by Science:1
“Researchers in four countries will soon start a clinical trial of an unorthodox approach to the new coronavirus. They will test whether a century-old vaccine against tuberculosis (TB), a bacterial disease, can rev up the human immune system in a broad way, allowing it to better fight the virus that causes coronavirus disease 2019 and, perhaps, prevent infection with it altogether.”
In April 2020, the measles-mumps-rubella (MMR) vaccine was touted as a “major breakthrough” against COVID-19. The British Express reported:2
“Researchers at the University of Cambridge said the injection could prevent severe symptoms in people who have had it because the rubella virus has a similar structure to the coronavirus …
When they compared the rubella virus and the coronavirus the researchers found that they were 29 percent identical … The researchers have no evidence that the MMR vaccine works on COVID-19 patients but they assured ‘a study is warranted.’”
In June 2020, it was the polio vaccine’s turn in the spotlight. According to The Hill,3 tuberculosis and polio vaccines are being examined “for possible protection against COVID-19.”
Jeffrey D. Cirillo, a professor of microbial pathogenesis and immunology at Texas A&M Health Science Center, went so far as to state, “This is the only vaccine in the world that can be given to combat COVID-19 right now.”
Based on what? Based on vaccination rates in countries such as Pakistan, “where most of the population is vaccinated for tuberculosis and death rates for COVID-19 have been extremely low.” That’s it.
Meanwhile, discussions and evidence showing the benefits of vitamin C and vitamin D — as well as many other therapies — are banned and censored. This, despite significant scientific evidence actually backing their use and showing the biology by which these nutrients and therapies can prevent and/or treat this particular infection. Talk about travesty.
The oral polio vaccine, by the way, is now the primary cause of polio paralysis in the world, not wild polio.4,5 This is an inconvenient fact that is completely ignored by most mainstream media.
In related news, June 12, 2020, the Daily Mail,6 Science Times7 and others8 reported findings from a Singaporean study9 led by professor Antonio Bertoletti, an immunologist with the Duke-NUS Medical School, showing common colds caused by the betacoronaviruses OC43 and HKU1 might make you more resistant to SARS-CoV-2 infection, and that the resulting immunity might last as long as 17 years.
In addition to the common cold, OC43 and HKU1 — two of the most commonly encountered betacoronaviruses10 — are also known to cause bronchitis, acute exacerbation of chronic obstructive pulmonary disease and pneumonia in all age groups.11 As reported by the Daily Mail:12
“They share many genetic features with the coronaviruses Covid-19, MERS and SARS, all of which passed from animals to humans. Coronaviruses are thought to account for up to 30 percent of all colds but it is not known specifically how many are caused by the betacoronavirus types.
Now scientists have found evidence that some immunity may be present for many years due to the body's 'memory' T-cells from attacks by previous viruses with a similar genetic make-up — even among people who have had no known exposure to Covid-19 or SARS …
Blood was taken from 24 patients who had recovered from Covid-19, 23 who had become ill from SARS and 18 who had never been exposed to either SARS or Covid-19 …
Half of patients in the group with no exposure to either Covid-19 or SARS possessed T-cells which showed immune response to the animal betacoronaviruses, Covid-19 and SARS. This suggested patients' immunity developed after exposure to common colds caused by betacoronavirus or possibly from other as yet unknown pathogens.”
In other words, if you’ve beat a common cold caused by a OC43 or HKU1 betacoronavirus in the past, you may have a 50/50 chance of having defensive T-cells that can recognize and help defend against SARS-CoV-2, the novel coronavirus that causes COVID-19. According to the researchers:13
“These findings demonstrate that virus-specific memory T-cells induced by betacoronavirus infection are long-lasting, which supports the notion that Covid-19 patients would develop long-term T-cell immunity. Our findings also raise the intriguing possibility that infection with related viruses can also protect from or modify the pathology caused by SARS-Cov-2.”
Other studies have also discovered that many appear to have prior resistance to SARS-CoV-2. For example, a study14 published May 14, 2020, in the journal Cell, found 70% of samples obtained by the La Jolla Institute for Immunology from patients who had recovered from mild cases of COVID-19, as well as 40% to 60% of people who had not been exposed to the virus, had resistance to SARS-CoV-2 on the T-cell level.
According to the authors, this suggests there’s “cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.” Like Bertoletti’s study above, the Cell study found that exposure to coronaviruses responsible for the common cold appear to allow your immune system to recognize and fight off SARS-CoV-2 as well.
May 14, 2020, Science magazine reported15 these Cell findings, drawing parallels to another earlier paper16 by German investigators that had come to a similar conclusion.
That German paper,17 the preprint of which was posted April 22, 2020, on Medrxiv, found helper T cells that targeted the SARS-CoV-2 spike protein in 15 of 18 patients hospitalized with COVID-19. As reported by Science:18
“The teams also asked whether people who haven’t been infected with SARS-CoV-2 also produce cells that combat it. Thiel and colleagues19 analyzed blood from 68 uninfected people and found that 34% hosted helper T cells that recognized SARS-CoV-2.
The La Jolla team20 detected this crossreactivity in about half of stored blood samples collected between 2015 and 2018, well before the current pandemic began …
The results suggest ‘one reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,’ says viral immunologist Steven Varga of the University of Iowa. However, neither of the studies attempted to establish that people with crossreactivity don’t become as ill from COVID-19.
Before these studies, researchers didn’t know whether T cells played a role in eliminating SARS-CoV-2, or even whether they could provoke a dangerous immune system overreaction. ‘These papers are really helpful because they start to define the T cell component of the immune response,’ [Columbia University virologist Angela] Rasmussen says.”
These studies add support to the latest COVID-19 mortality models suggesting widespread resistance and prior immunity. Freddie Sayers, executive editor of UnHerd, recently interviewed professor Karl Friston, a statistician whose expertise is mathematical modeling, who believes prior immunity across the global population might be as high as 80%. Sayers reports:21
“[Friston] invented the now standard ‘statistical parametric mapping’ technique for understanding brain imaging — and for the past months he has been applying his particular method of Bayesian analysis, which he calls ‘dynamic causal modelling,’ to the available Covid-19 data …
His models suggest that the stark difference between outcomes in the UK and Germany, for example, is not primarily an effect of different government actions (such as … earlier lockdowns), but is better explained by intrinsic differences between the populations that make the ‘susceptible population’ in Germany ... much smaller than in the UK ...
Even within the UK, the numbers point to the same thing: that the ‘effective susceptible population’ was never 100%, and was at most 50% and probably more like only 20% of the population.”
These statistics really throw the idea of social distancing being an unavoidable part of the post-COVID-19 “new normal” into question. What’s more, once sensible behaviors such as staying home when sick are entered into Friston’s model, the effect of lockdown efforts vanish altogether, so global lockdowns were likely completely unnecessary in the first place.
Michael Levitt,22 a professor of structural biology at the Stanford School of Medicine who received the Nobel Prize in 2013 for his development of multiscale models for complex chemical systems, has also presented strong evidence that supports Friston’s model.
According to Levitt, statistical data reveals a mathematical pattern that has stayed consistent regardless of the government interventions implemented. While early models predicted an exponential explosion of COVID-19 deaths, those predictions never materialized. As reported by Sayers in the video above:
“After around a two-week exponential growth of cases (and, subsequently, deaths) some kind of break kicks in, and growth starts slowing down. The curve quickly becomes ‘sub-exponential.’ This may seem like a technical distinction, but its implications are profound.
The ‘unmitigated’ scenarios modelled by (among others) Imperial College, and which tilted governments across the world into drastic action, relied on a presumption of continued exponential growth …
But Professor Levitt’s point is that that hasn’t actually happened anywhere, even in countries that have been relatively lax in their responses.”
Levitt believes prior immunity plays a significant role in why we simply don’t see an exponential growth pattern of COVID-19 deaths, and that certainly seems to make sense. A majority of people simply aren’t (and weren’t) susceptible to the disease in the first place.
He tells Sayers the indiscriminate lockdowns implemented around the world were “a huge mistake.” A more rational approach would have been to protect and isolate the elderly, who are by far the most vulnerable and make up the bulk of COVID-19 deaths around the world.
Hopefully, these data will not be swept under the rug if or when a second wave of COVID-19 emerges this fall. Making that mistake once is bad enough. Let us not repeat it.
Last but not least, to bolster your immune system and lower your risk of COVID-19 infection in the future, be sure to follow the instructions given in “Your Vitamin D Level Must Reach 60 ng/mL Before the Second Wave.”
In the top 10 leading causes of death listed by the Centers for Disease Control and Prevention, diabetes and high blood pressure contribute to or are the cause of five — heart disease, stroke, Alzheimer's disease, diabetes and kidney disease.1 In 2017, the American College of Cardiology and the American Heart Association redefined the parameters for high blood pressure.2
The change wasn't arbitrary. It was based on data showing that people with blood pressure measurements once considered normal were experiencing some of the same health complications as those who had high blood pressure.
When the new high blood pressure marker was lowered from 140/90 to 130/80, the American Heart Association estimated the number of people with high blood pressure jumped from 32% of the U.S. population to 46%.
This change was similar to a 2004 move by an international committee of experts who lowered the diagnosis of prediabetes from a blood glucose of 110 mg/dl to 100 mg/dl.3 As one researcher writes in Diabetes Care:4
"In the past it was thought that the cut point for diabetes represented a precise threshold of risk for microvascular complications, but it is clear that no such thresholds exist."
In 2018, there were 34.2 million in the U.S. with diabetes, according to the American Diabetes Association. Of these, 26.8 million had been diagnosed and 7.3 were estimated to be undiagnosed. As with many chronic conditions, diabetes is found more frequently in older adults.
Out of the 10.5% of the overall population with diabetes or prediabetes, 14.3 million people over 65 have one of the two chronic conditions.5 However, the overall numbers may be higher since data from 2019 showed that 87.8% of the U.S. population were metabolically inflexible,6 indicating some degree of insulin resistance,7,8 the hallmark of diabetes.
Doctors in China quickly realized after beginning to treat patients with COVID-19 that nearly half of those who were dying also had high blood pressure (hypertension).9 Researchers used retrospective data from a hospital dedicated only to the treatment of the infection in Wuhan, China, to evaluate the association.10
An analysis of 2,877 patients was done; this included 29.5% of whom had a history of high blood pressure. They found that those with high blood pressure had double the risk of dying compared to those who didn't. This included patients who had a history of high blood pressure but were not taking any medications.
Reports from other countries have also shown that people with high blood pressure are at higher risk from COVID-19.11 In the past it's been suggested that ACE inhibitors, which are medications to treat high blood pressure, can increase an individual's risk of severe disease.
More recent research has shown this is not the case.12 This is supported by a recent study published in the European Heart Journal. Scientists found the death rate among individuals using medications that affect the renin-angiotensin-aldosterone system inhibitors (RAAS), which include ACE inhibitors, are similar to those who do not take RAAS inhibitors. The researchers concluded:13
"While hypertension and the discontinuation of antihypertensive treatment are suspected to be related to increased risk of mortality, in this retrospective observational analysis, we did not detect any harm of RAAS inhibitors in patients infected with COVID-19."
As reported by Reuters,14 the researchers were surprised the results of their analysis showed a trend in favor of patients using ACE inhibitors. They included their data with past studies and found a blood pressure medication may be associated with a reduced risk of mortality.
A second comorbidity with an increased rate of severe disease and mortality is diabetes. Researchers gathered data from the National Health Service England to characterize the features of U.K. individuals who may experience severe COVID-19.15
The information came from 166 hospitals from February 6, 2020, to April 18, 2020. The researchers used a preapproved questionnaire from the World Health Organization that reported many of the study participants were also enrolled in other clinical trials and interventional studies.
The data showed the median age of individuals hospitalized for COVID-19 was 72 years with a hospital stay of about seven days. The most common comorbidities were chronic heart disease, diabetes and chronic pulmonary disease.
Thus far, it's been unclear as to whether people with diabetes are more likely to get infected, but what is clear is that a disproportionate number with diabetes are hospitalized with severe illness. It's been estimated that 6% of the U.K. population has diabetes,16 but data from the NHS England showed that 19% of those hospitalized had diabetes,17 which is nearly three times the number in the general population.
It's also important to note that while people with Type 2 diabetes have double the risk of dying from COVID-19, people with Type 1 diabetes are 3.5 times more likely to die from the virus than people without diabetes.18
In another study of 174 patients, scientists found that those with diabetes had a higher risk of severe pneumonia, excessive uncontrolled inflammation and dysregulation of glucose metabolism.19 They concluded that their data supported the idea that those with diabetes may experience a rapid progression of COVID-19 and that they will have a poor prognosis.
One team from Brown University believes the reasons behind certain people being hit harder by the virus may be a function of androgenic activity, which has to do with male hormones. The team conducted two studies in Spain.20
In the first, they evaluated the results of 41 Caucasian males who were admitted to the hospital with bilateral pneumonia and who were positive for SARS-CoV-2. In this group, 71% had clinically significant androgenic alopecia (AGA).21
The prevalence of AGA in Spanish Caucasian males is unknown; however, the researchers expected a prevalence of up to 53%. In this study, the researchers only visually diagnosed AGA and did not speak with the individuals. They hypothesized that if AGA could be confirmed as a risk factor, then an anti-androgen therapy may help reduce the severity of symptoms:22
"… recent attention to the anti‐malarial drug hydroxychloroquine is of interest. Chloroquine phosphate, an analogue of hydroxychloroquine, has been demonstrated to reduce testosterone in rodents … Although the data supporting the use of hydroxychloroquine for treatment of COVID‐19 is limited and the potential negative side effects in COVID‐19 patients are unknown, the connection to androgens may prove important."
Recognizing the initial study had a small sample size, the research team undertook a second analysis of data that were published in the Journal of the American Academy of Dermatology.23 In this study, a dermatologist diagnosed AGA in a cohort of 175 individuals, 122 of whom were males and 53 of whom were females; 79% of the men had AGA and 42% of the women had it.
It's important to know that the median age of the women was 71, whereas with men it was 62.5 years. Again, the researchers found a substantial percentage of people in the hospital with severe disease had AGA.
AGA is also known as male pattern baldness, and in women it's called female-pattern hair loss.24 Diagnosis is made on a history and examination evaluating for risk factors, which include advancing age, polycystic ovary syndrome, insulin resistance and prostate cancer.
The underlying factor common to each of these chronic health conditions associated with severe COVID-19 is insulin resistance. The researchers from Brown University acknowledge their patient population included older adults, who are known to be at higher risk of severe disease.
In other studies, researchers have identified obesity as a prominent risk factor, as it doubles the risk of hospitalization in people under 60 with COVID-19.25 While obesity is at the top of the list, another investigation shows individuals with more severe disease have more than one underlying health condition.
A study involving 5,700 New York City patients26 produced results showing that the most common comorbidities were high blood pressure,27 obesity28 and diabetes, all of which are related to insulin resistance. In the study group, 56.6% had high blood pressure, 41.7% were obese and 33.8% had diabetes.
In the group of patients who died, the researchers found that those who had diabetes had a higher likelihood of being on mechanical ventilation or placed in the ICU compared to those who did not. Interestingly, those who had high blood pressure were less likely to have been on a ventilator or in an ICU before they died, compared to those who did not have high blood pressure.
Higher glucose levels, a hallmark of Type 2 diabetes, insulin resistance and metabolic syndrome, appear to play significant roles in viral replication and the development of cytokine storms, which are known to occur in severe COVID-19. For further discussion and more information, see "The Real Pandemic Is Insulin Resistance."
It appears that people have come to accept the growing number who suffer from high blood pressure, diabetes and cardiovascular diseases as a normal part of living in Western society. However, these chronic diseases are not normal at all, regardless of age.
To survive the next pandemic, whatever that might be, improving public health must be the priority. It's unreasonable to wait for a drug or vaccine to cure what your body can naturally fight. Instead of throwing drugs at symptoms, it's time to address the underlying causes of illness and disease.
Supporting a robust immune function is necessary to effectively combat COVID-19, flu, the common cold and most other infectious diseases. Addressing insulin resistance is the key to reducing chronic disease and improving health.
To do that, it's necessary to dramatically cut down on processed foods and increase the amount of whole foods eaten. Dr. Sandra Weber, president of the American Association of Clinical Endocrinologists, commented in the New York Times:29
"We know that if you do not have good glucose control, you're at high risk for infection, including viruses and presumably this one [COVID-19] as well … [improving glucose control] would put you in a situation where you would have better immune function."
For details on what and when to eat to reverse insulin resistance, see "Want to Defeat Coronavirus? Address Diabetes and Hypertension." In that article, I also summarize several key strategies for getting and staying healthy and metabolically fit. For additional COVID-19 remedies and top tips, see my Coronavirus Resource Page.
If you'd like a more in-depth understanding of how to become metabolically flexible and eliminate insulin resistance, consider getting a copy of my book. "Fat for Fuel." It goes into detail, providing a comprehensive program to help optimize metabolic flexibility and strengthen your immune system. Both are crucial components of health and disease prevention.
