The controversy over alcohol consumption: Is it good or bad for your heart?

June 13, 2022June 10, 2022 Huan Wang, PhD

If you go to a party or a professional event, you won’t be surprised to find that alcoholic beverages are served. In fact, in most cases, it’s even expected. Alcohol consumption has been present throughout human history. So do its effects. Excessive drinking has been linked to many health risks, including high blood pressure, heart diseases, stroke, liver diseases, and digestive problems. However, the health effects of light-to-moderate drinking are still in dispute (1). Early evidence showed that light-to-moderate drinking is associated with beneficial effects such as reductions in coronary artery diseases and even in total mortality. This view has been challenged by a few recently published epidemiological studies, which show no direct relationship between the beneficial effects on the heart and light-to-moderate drinking (2).

What is light/moderate drinking?

According to National Institute on Alcohol Abuse & Alcoholism, moderate drinking is up to four alcoholic drinks for men and three for women in any single day and a maximum of 14 drinks for men and 7 drinks for women per week. Below that range would be considered light drinking.

Why is there a discrepancy in health risks reports on alcohol consumption?

The obvious:

Confounding factors such as social-economic status, age, genetics, ethnicities, behavior and types of alcoholic beverages play big roles in influencing health effects. It’s not hard to imagine that a wealthy family has more medical resources and more options of choosing a healthy lifestyle, which has lower risks of cardiovascular diseases compared to a low social-economic status family that even consumes the same amount of alcohol. The alcohol metabolism rate differs in different age groups and different populations. The certain population lacks an enzyme, alcohol dehydrogenase, which metabolizes alcohol, that has adverse health effects when drinking alcohol. These confounding factors are important when conducting an epidemiology study. Not all alcoholic drinks are created equal. Bioactive phytochemicals, for example, polyphenols have beneficial effects which can be found in wines. Cocktails usually contain a large amount of sugar, and high sugar consumption are linked to many cardiovascular disorders. It’s hard to tease out the causal effects of light-to-moderate alcohol consumption and the health effects. Moreover, most of the reported works of literature are observational, which leads to more complications when trying to interpret the data.

The less obvious:

Epidemiological study design has evolved rapidly in recent decades. Early studies were focused on interpreting results from limited resources. The lack of enough participants and missing specific details make it impossible to make a causal connection between alcohol consumption and health risks. In 2007, researchers started to encourage epidemiological studies to use large, prospective, and randomized trials when trying to understand the health effects of drinking (3). A recent review just published in Circulation: Heart failure questioned the relationship between alcohol intake and cardiomyopathy and heart failure (4). After analyzing current evidence, they suggest that there is no consensus on the absolute amount alcohol intake which causes cardiomyopathy and heart failure. Another group showed that low alcohol intake has no health benefits, and moderate alcohol intake is associated with adverse effects in heart (5).

To drink or not to drink. There is no one-size-fits-all solution. The jury is still out when it comes to the health effects of light-to-moderate drinking. Monitor your health and consult with your doctor regularly. If it’s not good for you, your body will tell.

REFERENCE

Piano, M. R. (2017). Alcohol’s Effects on the Cardiovascular System.Alcohol Research : Current Reviews, 38(2), 219–241.
Biddinger, K. J., Emdin, C. A., Haas, M. E., Wang, M., Hindy, G., Ellinor, P. T., Kathiresan, S., Khera, A. v, & Aragam, K. G. (2022). Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease.JAMA Network Open, 5(3), e223849–e223849.
Kloner, R. A., & Rezkalla, S. H. (2007). To Drink or Not to Drink? That Is the Question.Circulation, 116(11), 1306–1317.
Andersson, C., Schou, M., Gustafsson, F., & Torp-Pedersen, C. (2022). Alcohol Intake in Patients With Cardiomyopathy and Heart Failure: Consensus and Controversy.Circulation: Heart Failure, 0(0), 10.1161/CIRCHEARTFAILURE.121.009459.
The abstract ‘Moderate alcohol consumption is associated with progression of left ventricular dysfunction in a European stage B heart failure population’ will be presented during the session ‘Heart failure is a complex syndrome: look at comorbidities’ which takes place on 22 May at 09:40 CEST at Moderated ePoster 1.

“The views, opinions, and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness, and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions, or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your health matters. If you think you are having a heart attack, stroke, or another emergency, please call 911 immediately.”

Fast Forward to Spring, Slowly Fall Back to the Normal Heart

March 23, 2022March 22, 2022 Huan Wang, PhD

As the days become longer and the weather gets warmer, it’s that time of year again. Daylight saving time has been observed in most parts of the United States, and it’s time to manually set the clock one hour forward. When the clocks go forward, we ‘lose’ one hour of sleep. Even you try to compensate by forcing yourself to sleep more, your body might not follow your brain’s instructions due to the constant biological clock system, circadian rhythms. In a simple way, sudden disruption of sleep schedule could cause sleep deprivation and misalignment. The consequences of sleep disruption could have profound impacts, especially on cardiovascular health.

Why do we have daylight saving time?

In the United States, it’s scheduled to be the second weekend of March. In the European countries, the daylight saving normally is on the last weekend of March in spring. The idea is pretty much the same. The origin of daylight saving dated back to 1784, Benjamin Franklin proposed to adjust clocks for economic reasons. About 130 years later, Great Britain started to enact the daylight-saving rule to reduce energy costs during the war. Other countries then followed suit.

What are the health consequences?

One of the main consequences of forwarding one hour of clocks is sleep disruption. Despite the common opinion that shifting one hour of sleep ahead is inconsequential, increased sleep fragmentation and sleep latency present a cumulative effect of sleep loss at least across the following week, possibly longer (1). Circadian rhythms, commonly known as the internal clock, can directly or indirectly regulate many important biological functions such as sleep and locomotor activities, feeding and drinking behavior, core body temperature, endocrine activity, metabolism, autonomic and sympathetic activity, and many others (2).

What can we do to mediate the effects?

In 2020, the American Academy of Sleep Medicine published a statement calling for the abolition of daylight saving (3). It discussed acute and chronic harmful effects of sudden transition of sleep schedule attributed to daylight saving. The academy said, “the shift, by disrupting the body’s natural clock, could cause an increased risk of stroke and cardiovascular events, and could lead to more traffic accidents”. A call for permanent daylight saving time has been advocated and discussed both in European countries and in the United States. Just recently, United States senates approved a bill to make daylight saving permeant, the Sunshine Protection Act. Whether it will get approved by the House of Representatives and President Joe Biden, it’s still unknown.

At the moment, there are a few approaches to facilitate a smooth transition to the spring season. Common practices of good sleep hygiene such as avoiding caffeine and alcohol consumption late at night, following a consistent sleep schedule, using relaxation techniques to facilitate a stress-free sleep, avoiding screen exposure before bed, avoiding eating too close to bedtime would be some good starts. It’s also recommended to adjust clock time gradually to the daylight saving time a few days before and increase morning sun exposure to facilitate internal clock re-adjustment after daylight saving. Don’t expect your body can suddenly adjust to a new time schedule, treat it like jet lag. Allow some time for your body to recover and take it slowly to be your normal self.

REFERENCE

Manfredini, R., Fabbian, F., Cappadona, R., & Modesti, P. A. (2018). Daylight saving time, circadian rhythms, and cardiovascular health. Internal and Emergency Medicine, 13(5), 641–646.
Young, M. E., & Bray, M. S. (2007). Potential role for peripheral circadian clock dyssynchrony in the pathogenesis of cardiovascular dysfunction. Sleep Medicine, 8(6), 656–667.
Rishi MA, Ahmed O, Barrantes Perez JH, et al. Daylight saving time: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2020;16(10):1781–1784.

Vascular Discovery 2022: From Genes to Medicine

March 3, 2022February 22, 2022 Huan Wang, PhD

Have you been lingering on what else is going on within the field of atherosclerosis research after this year’s Scientific Sessions in American Heart Association? You might want to check out Vascular Discovery 2022, a 2 ½-day meeting, which is sponsored by the Council on Arteriosclerosis, Thrombosis and Vascular Biology, the Peripheral Vascular Disease Council, and the Council on Genomic and Precision Medicine, in cooperation with and the Society for Vascular Surgery’s Vascular Research Initiatives Conference (Flyer on the right).

What is the conference about?

The primary goal of the Vascular Discovery: From Genes to Medicine Scientific Sessions is to provide a forum for the timely exchange of information about new and emerging scientific research in lipids and lipoproteins, arteriosclerosis, thrombosis, vascular biology, genomics, precision medicine, peripheral vascular disease, and vascular surgery.

One of the long-standing objectives of this conference is to provide a unique platform for colleagues to build valuable networks, establish potential collaborations and promote early career scientists via providing role model inspirations and mentorship opportunities. The advantages of direct social interactions are indisputable, especially when it comes to build meaningful relationships. This year’s Vascular Discovery will be held in-person in Seattle. It will bring colleagues from worldwide, share groundbreaking science and bridge different disciplines in a classic old fashion way.

Who should attend?

This event will appeal to scientists and clinicians in cardiovascular medicine, cardiovascular research, thrombosis research, clinical cardiology, molecular/cellular biology, vascular biology, vascular medicine, vascular surgery, endocrinology, genetics, functional genomics, hematology, immunology, nutrition, and physiology.

Past highlights and feature events

While the planning committee is finalizing the abstracts and awardees, we can take a glimpse of what happened in 2021, which will shed some lights into the 2022 scientistic sessions. Vascular Discovery presented a virtual experience to the attendees in 2021, because of COVID pandemics. Since COVID has been the primary attention in public and scientific communities the past couple years, one of the important focuses of Vascular Discovery 2021 is on understanding how COVID-19 affects vascular systems, to identify who and when to treat patients in vascular research and clinical trials. Other important discussions are on identifying new approaches to understand the pathophysiology of atherosclerosis via risk factor identifications, and a distinguished lecture was presented by Marlene Rabinovitch, M.D. on multiple approaches of identifying a therapeutic target for treating pulmonary hypertension. More highlights are shown in the American Heart Association website¹.

Are you excited about attending this year’s in-person Vascular Discovery: from Genes to Medicine Scientific Sessions in Seattle? Stay tuned on the latest programming of 2022, which hopefully will be finalized and released in early March.

Registration for the Vascular Discovery Conference is now open. Early Bird pricing closes on 3/31, and Advance pricing opens on 4/1. Register now for the best price!

REFERENCE

1. American Heart Association. Science News 2021. https://professional.heart.org/en/meetings/vascular-discovery-from-genes

The darkness before the dawn–Long COVID is lurking around

January 24, 2022January 21, 2022 Huan Wang, PhD

As we are starting to live with the facts that COVID-19 is not leaving us any time soon, sense of danger and urgency start to fade away. More than two years have passed, we have made great strides in combating the pandemics. With advanced technologies, vaccine and antiviral drug developments provide us potential means out of this seemingly never-ending battle. Viruses constantly change through mutation. While Delta variant is phasing out, Omicron variant begins its domination globally. Current research suggest that Omicron variant is less deadly compared to the Delta variant, especially to fully vaccinated people. However, the high spread rate of Omicron variant is a major concern to the public.

Some of us may wonder, it might not be a big deal. Since most evidence suggest that the symptoms of fully vaccinated patients are rather minor, especially the chance of suffering severe symptoms if you had a booster shot is even less. After a few days discomfort, you might end up obtaining better immunity after building up antibodies through infection. It might be partially true to some people. However, some unlucky ones continue to suffer from post-COVID conditions even after four or more weeks. These post-COVID conditions are also known as long COVID, long-haul COVID, post-acute COVID, long-term effects of COVID, or chronic COVID.

What is long COVID?

According to the US Centers for Disease Control and Prevention (CDC), long COVID describes the condition as sequelae that extend beyond four weeks after initial infection¹. The timeline of post-acute COVID-19 shows as Fig1. The list of common symptoms of post-COVID conditions is growing. Symptoms which people commonly report include difficulty breathing, fatigue, brain fog, cough, chest/stomach pain, headache, heart palpitations, muscle pain, diarrhea, sleep problems, fever, lightheadedness, rash, mood changes, changes in smell or taste, and changes in menstrual period cycles^2,3. The challenges of diagnosing long COVID are multiple layers. The social isolation resulting from pandemic prevention measures can cause mental health stress such as depression, anxiety, and mood changes. Complications of pre-existing conditions may unmask after COVID infections. Reinfection of COVID could be mistaken as persistent symptoms. Multiple organs are reported being the victims of SARS-CoV-2 infection, for example, lungs, heart, brain, kidney, spleen, liver and the cardiovascular systems⁴ (Fig2). Some people have severe illness with COVID experience combinations of multiorgan effects or autoimmune conditions with symptoms lasting for weeks or months after initial infection. Long COVID is a serious concern. We just begin to understand it, and the path to be able to treat it with ease is winding.

Various guidelines have been established focus on treating and managing COVID^5,6 and long COVID⁷. While the guidelines will undoubtedly improve as new evidence comes to light. The etiology, mechanism, and consequences of COVID and long COVID remain elusive currently. Large epidemiology studies are undergoing to help us understand mechanisms and develop targeted treatments. American Heart Association just establishes a new funding program to invite more researchers to study the mechanisms underlying cardiovascular consequences associated with COVID-19 and long COVID in January 2022. Scientific communities are racing to understand COVID and long COVID.

The COVID pandemics is a serious public crisis. Although the situation may seem be getting better, healthcare staff shortages caused by pervasive Omicron variant infections and the lack of rapid COVID tests are posing imminent danger to the public healthcare system. Moreover, the effects of long COVID vary person by person, it’s better to stay vigilant and not get infected than taking it callously and passing it to vulnerable people unintentionally.

REFERECE

Datta SD, Talwar A, Lee JT. A Proposed Framework and Timeline of the Spectrum of Disease Due to SARS-CoV-2 Infection: Illness Beyond Acute Infection and Public Health Implications. JAMA. 2020;324(22):2251–2252.
Al-Aly Z, Xie Y, Bowe B. High-dimensional characterization of post-acute sequelae of COVID-19. Nature. 2021;594(7862):259–264.
Nalbandian A, Sehgal K, Gupta A, Madhavan M V, McGroder C, Stevens JS, Cook JR, Nordvig AS, Shalev D, Sehrawat TS, Ahluwalia N, Bikdeli B, Dietz D, Der-Nigoghossian C, Liyanage-Don N, et al. Post-acute COVID-19 syndrome. Nature Medicine. 2021;27(4):601–615.
Crook H, Raza S, Nowell J, Young M, Edison P. Long covid–mechanisms, risk factors, and management. BMJ. 2021;374.
World Health Organization. COVID-19 clinical management: living guidance. 2021. https://www.who.int/publications/i/item/WHO-2019-nCoV-clinical-2021-1
National Institute of Health. Coronavirus disease 2019 (COVID-19) treatment guidelines. 2021. https://www.covid19treatmentguidelines.nih.gov/
National Institute for Health and Care Excellence. COVID-19 rapid guideline: managing the long-term effects of COVID-19 NICE guideline; c2020. https://www.nice.org.uk/guidance/ng188

The New Phase of the Prevention Pyramid–the Primordial Prevention

December 22, 2021December 17, 2021 Huan Wang, PhD

You are what your mother eats: launch a new generation into a lifetime of ideal cardiovascular health

––#AHA21 Recap from presidential lecture by Dr. Don Lloyd-Jones, AHA President

My PhD research was focused on maternal nutrition and epigenetics. When I started graduate school, the field of epigenetics just started to make some splash in the scientific community. As a new graduate student, I have a plethora of questions. What is epigenetics? Why should I care to study it? How does that have anything to do with nutrition? You are what your mother ate. The food your mother had during pregnancy and lactation can forever change your health through epigenetic regulation (without changes in your genetic makeup). This became my passion, to understand how maternal nutrition affects offspring and how to promote healthy life from the beginning of everything.

At 2021 scientific sessions of American Heart Association (AHA), Dr. Don Lloyd-Jones gave an inspirational speech about the next phase of the Prevention Pyramid–the Primordial Prevention (Fig.1). The previous Prevention Pyramid contains three segments which were chronically progressed: Tertiary Prevention,

Secondary Prevention, and Primary Prevention. With the development of medical devices and acute therapy, the Tertiary Prevention helped in-hospital mortality rate drop from more than 30% to less than 5%. The Secondary Prevention applies discharge therapies and significantly reduces the recurrent incidences of cardiovascular diseases (CVD) events. The current strategy to fight CVD is through reducing incidences via targeting risk factors, called the Primary Prevention. Starting from the Framingham Heart Study, many important risk factors of CVD such as age, blood cholesterol level, blood pressure, smoking status have been identified. The previous Prevention pyramid made a big success in terms of CVD prevention until 2011. Then the progress curve starts to show stagnation, partly because of obesity epidemics sequelae and widening social-economics disparities.

With the help of pioneer research from Dr. Jeremiah Stamler from Northwestern University, modern CVD studies start to shift focus to study healthy people for low risk factor identification. AHA developed criteria, “Life’s simple 7^TM” , defining ideal cardiovascular health (CVH): stop smoking, eat better, get active, lose weight, manage blood pressure, control cholesterol, and reduce blood sugar¹. High CVH is associate with better CVD events prevention, the CVH trajectories from childhood are set as early as the 3^rd grade². Current research showed that women with ideal maternal gestational CVH is 8+ times more likely to have offspring with ideal CVH 10 years later³. The importance of Primordial Prevention is unignorable. From the latest discoveries of epigenetics studies, results suggest that not only mother’s CVH can affect babies’ CVH, father’s CVH could potentially possess certain influences as well⁴.

“No man is an island”, as John Donne wrote. Social determinants of health can affect 80% to 90% of a person’s risk factors (Fig. 2). To promote a better CVH for the whole community, AHA relentlessly aims to drive a more equitable health impact to the society. “Let’s do this for all the children in our life”, as Dr. Lloyd-Jones concluded, AHA is dedicating funding for more research studies to guide us towards an exciting phase of CVD prevention, the Primordial Prevention in the foreseeable future.

REFERENCES

Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK, Fonarow GC, Ho PM, Lauer MS, Masoudi FA, et al. Defining and Setting National Goals for Cardiovascular Health Promotion and Disease Reduction. Circulation. 2010;121(4):586–613.
Allen NB, Krefman AE, Labarthe D, Greenland P, Juonala M, Kähönen M, Lehtimäki T, Day RS, Bazzano LA, Van Horn L V, Liu L, Alonso CF, Webber LS, Pahkala K, Laitinen TT, et al. Cardiovascular Health Trajectories From Childhood Through Middle Age and Their Association With Subclinical Atherosclerosis. JAMA Cardiology. 2020;5(5):557–566.
Perak AM, Lancki N, Kuang A, Labarthe DR, Allen NB, Shah SH, Lowe LP, Grobman WA, Lawrence JM, Lloyd-Jones DM, Lowe Jr WL, Scholtens DM, Group HF-USCR. Associations of Maternal Cardiovascular Health in Pregnancy With Offspring Cardiovascular Health in Early Adolescence. JAMA. 2021;325(7):658–668.
Hughes V. Epigenetics: The sins of the father. Nature. 2014;507(7490):22–24.

“The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.”

How to Protect Your Aging Heart

November 14, 2021November 14, 2021 Huan Wang, PhD

“Man is as old as his arteries.” –Thomas Sydenham

Cardiovascular diseases are commonly associated with unhealthy lifestyles. Do you know that age is a strong predictor of cardiovascular diseases in both men and women? As you grow older, your risks of suffering a heart attack, to have a stroke, or to develop coronary heart disease and heart failure are getting much higher. Ageing research has been evolving rapidly in the recent decades. In the early days, ageing research was mostly focused on Alzheimer’s disease and related dementias. To improve quality of life in ageing population, other symptoms of ageing including physiological function decline start to capture scientific community’s attention. In AHA Scientific Sessions 2021, a panel of experts and professionals in the field talked about novel strategies to promote healthy vascular aging.

To prevent cardiovascular diseases in aging populations, there are many take-home messages from today’s live session. Dr. Blumenthal from Johns Hopkins University used a simple “ABCDEF” approach¹ to highlight the most recent development in cardiovascular diseases management based on most recent scientific discoveries and epidemiological results. Two of the major factors: Diet and Exercise, which are closely associated with body weight management, are further elaborated by Drs. Willett and Donato, respectively.

Dr. Willett is a professor of Epidemiology and Nutrition from Harvard Medical School. He challenged the recommendation of Dietary Guidelines for Americans (DGA). Dr. Willett encouraged the public to focus on evidence-based dietary recommendation, and to evaluate epidemiological studies by using randomized control trials with risk factor, disease incidence and mortality outcomes and prospective epidemiological studies with equal intensity intervention of 12-month and longer. Aside from canonical discussion of dietary recommendation based on health benefits, Dr. Willett raised a pertinent point in environmental sustainability. “How to feed 2 billion people in 2050?” he asked. Climate change is a global crisis and agriculture plays a pivotal role in fighting it. In “the Omnivore’s Dilemma”, Michael Pollan talked about how livestock production is responsible for much of the carbon footprint of global agriculture. The best practice for specific diets to prolong healthy life needs to take into consideration of reducing carbon footprint.

Vascular ageing is comprised of multiple processes including cellular senescence, inflammation and oxidative stress². Dr. Donato talked about how ageing affects endothelial cell function and habitual aerobic exercise improves endothelial function in men. He also raised an interesting point: this beneficial effect of exercise on endothelial function is sex dependent. More research on sex differences needs to help us understand how to promote healthy ageing. DNA damage is associated with vascular aging. Dr. Shanahan discussed the signaling pathways involving in DNA damage and cellular senescence-associated phenotypes on vascular calcification. Inhibition of DNA damage agents can mediate vascular calcification progression. Can we use DNA damage as a biomarker to detect vascular ageing?

The “One-size-fits-for-all” approach in disease prevention and treatment requires a new perspective. In 2015, Precision Medicine Initiative was launched to accelerate research in disease treatment and prevention by considering individual differences in people’s genes, environments and lifestyles. With the development of next-generation sequencing, risk factors for coronary artery diseases require a modification. Dr. Wolford discussed her research on incorporating genetic backgrounds for disease prediction using polygenic risk scores³. It’s only the beginning of an exciting era using precision medicine as a tool for disease prevention and intervention in cardiovascular diseases.

To protect an aging heart, many approaches need to be implemented. Healthy lifestyles, nice environment and consideration of individual differences are all part of a clue.

REFERENCE

Feldman DI, Wu KC, Hays AG, Marvel FA, Martin SS, Blumenthal RS, Sharma G. The Johns Hopkins Ciccarone Center’s expanded ‘ABC’s approach to highlight 2020 updates in cardiovascular disease prevention. American Journal of Preventive Cardiology. 2021;6:100181.
Donato AJ, Machin DR, Lesniewski LA. Mechanisms of Dysfunction in the Aging Vasculature and Role in Age-Related Disease. Circulation Research. 2018;123(7):825–848.
Wolford BN, Surakka I, Graham SE, Nielsen JB, Zhou W, Gabrielsen ME, Skogholt AH, Brumpton BM, Douville N, Hornsby WE, Fritsche LG, Boehnke M, Lee S, Kang HM, Hveem K, et al. Utility of family history in disease prediction in the era of polygenic scores. medRxiv. 2021:2021.06.25.21259158.

Diet, Fat, and Healthy Heart

July 16, 2021July 7, 2021 Huan Wang, PhD

What type of milk do you prefer? Most people will give you their answers quickly without much hesitation. Besides taste and flavor, whether to choose whole milk (~3.5% fat), reduced-fat milk (2% fat) or skim milk (0% fat) depends mostly on how much fat do you prefer in your diet. Reduced fat milk and skim milk have become the poster children for heart beneficial diets in the past decades. The long-held belief that fat is bad for your heart originates from a famous epidemiology study conducted by Ancel Keys and colleagues¹.

Ancel Keys’ Seven Countries Studies influenced dietary recommendation on fat for decades. Keys believed that fatty foods such as dairy products and red meat are the culprit for coronary heart disease. He studied diet, lifestyle, and incidence of coronary heart diseases in about 13,000 adult men in Finland, Greece, Italy, Japan, the Netherlands, the United States, and Yugoslavia¹, and found that countries with diets high in saturated fat including the United States have the highest blood cholesterol levels and heart-attack death rates. Based on Keys’ studies and other similar findings, the United States and the United Kingdom introduced dietary guidelines which recommend reducing consumption of saturated fat to about 10% of total energy intake, to lower cholesterol in the blood and therefore decrease the risks of a heart attack. A low-fat diet has been associated with good health practices ever since. Here is a twist to this story, Keys didn’t include France, where the nation’s high-fat diet doesn’t correlate with the occurrence of heart diseases. It turns out to be the opposite.

Not all fat is created equal. Let’s take milk fat for example. Milk fat contains a variety of fats such as saturated fat, unsaturated fat, and trans-fat. Generally, trans-fat is considered as “bad” fat in processed foods and fried foods, however, naturally found trans-fat in milk is beneficial. Another example is cholesterol. It’s taken for granted to associate dysregulated blood cholesterol levels with dietary cholesterol intake. In fact, it’s not cholesterol itself that causes high blood cholesterol levels, but rather the lipoproteins that move cholesterol in and out of cells. Broadly, there are the “good” cholesterol– high-density lipoprotein (HDL) and the “bad” cholesterol– low-density and very-low-density lipoproteins (LDL and VLDL). Seventy percent of milk fat is saturated fat, and saturated fats in milk raise both HDL (good) and LDL (bad) cholesterol. The net effect of milk fat might be neutral. Processed foods, fried foods and stick margarine have lots of trans-fats from production and are known for raising LDL cholesterol and lowering HDL cholesterol.

The “good” and “bad” cholesterol levels are considered as the golden standard for cardiovascular risk prediction. However, recent research shows that high HDL levels in some cases associated with higher risks in heart disease². The plot is thickened. It turns out that some people with a genetic mutation in HDL receptor gene fail to transport cholesterol outside of blood, therefore results in higher level of fats in the body despite having high levels of HDL cholesterols in the circulation. In conclusion, blindly relying on fat content in the Nutrition label is simply not enough.

Now, let’s go back to the milk choice question one more time. Not only we need to consider what type of fat in cow milk, but we also need to look at other factors too. Sugar is often ignored when it comes to buying milk. Reduced fat and skim milk contain slightly more carbohydrates than whole fat milk does. If your goal is to lose weight by reducing fat content in your milk, you might get disappointed. The relationship between milk fat and weight management is still not clear. An epidemiology study shows that women who consumed more than 1 serving of whole fat milk per day were 15% less likely to gain weight compared to those who drink low fat milk³. Also recent research show that consuming saturated fat does not directly cause heart disease⁴. Therefore, how much you eat doesn’t necessarily translate to how much will end up in your body. It depends on how you body metabolizes it, what’s your genetic makeup and what else in your diet potentially positively or negatively contribute to the net outcomes. Last not the least, even not all fat creates equal, trans-fat from fried foods and processed foods are still universally considered bad for your health. Try to avoid those if it’s possible.

REFERENCE

Keys A. Seven Countries. Harvard University Press; 2013.
Zanoni P, Khetarpal SA, Larach DB, Hancock-Cerutti WF, Millar JS, Cuchel M, DerOhannessian S, Kontush A, Surendran P, Saleheen D, Trompet S, Jukema JW, De Craen A, Deloukas P, Sattar N, et al. Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease. Science. 2016;351(6278):1166 LP – 1171.
Rosell M, Håkansson NN, Wolk A. Association between dairy food consumption and weight change over 9 y in 19 352 perimenopausal women. The American Journal of Clinical Nutrition. 2006;84(6):1481–1488.
Weinberg SL. The diet–heart hypothesis: a critique. Journal of the American College of Cardiology. 2004;43(5):731–733.
“The facts on fats infographic” [Image] (2017). American Heart Association. https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/fats/the-facts-on-fats

Speak to Me: effective scientific communication

June 21, 2021June 16, 2021 Huan Wang, PhD

What is science communication? What are the differences between a research seminar and a TED-style talk? I recently had a chance to present my research discoveries in a very short (3min) format to fellow colleagues. It didn’t go as well as I planned. I noticed the varieties of styles and topics, so I decided to look into effective ways for science communication. “Science communication is defined as the use of appropriate skills, media, activities, and dialogue to produce one or more of the following personal responses to science: Awareness, Enjoyment, Interest, Opinion-forming, and Understanding”, a contemporary definition of science communication¹. Scientists are more aware of the importance of scientific communication in recent decades. The reasons for science communications range from grant requirements, public engagement, to feelings of moral obligation². Audiences are also very diverse such as interested/non-interested laypeople, engaged stakeholders and policymakers, and scientific colleagues from other disciplines.

Many articles discussed the techniques for effective science communication. They are very accessible through websites. An article published by Steven J. Cooke and colleagues shared a nice collection of useful websites in a table format with emphasis on key resources on science communication for scientists³. With a great wealth of information online, I’m going to share some major points regarding effective science communication.

Know your audiences

For any kind of effective science communication, the first step is to set objectives. Why are you interested in sharing what you know? What do you want your audiences to take home? Then the next question naturally will be who are your audiences? The knowledge depth of your audience decides how you want to present your story. Imagine a nuclear scientist tries to tell a government official that what is radioactive. Think critically about what aspect of your science will reach the target audience. It’s paramount that the information you share is of appropriate complexity. For example, you would describe your research differently to a group of colleagues than to high school students– and even specialized audiences like colleagues are not homogeneous. Some may specialize in a different field.

Avoid acronyms and jargons

One of the biggest obstacles to effective communication is acronyms and jargon. Imagine if you hear a spy uses morse code to communicate. It’s basically the same when a scientist uses his/her “comfortable languages” to talk to “insiders”. Sometimes it forms a special bond and feels very exclusive. Most of the time it saves lots of time and energy to repeat some concepts over and over. Scientific concepts sometimes could be less institutional. Avoid acronyms that could reach a broader audience. Regardless of what forms of communication, acronyms should be critically scrutinized based on necessity and commonality. Multidisciplinary studies embrace effective communication among scientists and acronyms are not going to make it easier. Jargon is a similar but different issue. If you look at the word panel in Fig1⁴. You might find some commonly used words by in the jargon category. When you bury yourself in your specialized field long enough, you might find it harder to distinguish what is jargon and what is not. A group scientists developed a program to help scientists identify jargons⁴ and there might be other resources online to achieve a similar goal.

Fig1: Screen shot showing words after de-jargoning4.

Focus on the science

It’s not a big surprise for scientists to think and talk about science all the time. Avoiding granular details is one of the top lessons I learned as a graduate student. If you practice this fashion in an extreme way, if could be counterproductive. Good science is the foundation of quality science communication. Don’t lose sight that people are interested in your talk/post because you have a unique science-based perspective. “Avoid patronizing an audience by oversimplifying or glossing over important scientific details, as interested people want to hear about the scientific process and see the data themselves.”³. An effective science communication should include appropriate details which covers significance, background, challenges, as well as results. Be creative, be relatable and be interesting. Most importantly, be true to the data and don’t oversell or overstate the results. Share with the audiences your enthusiasm based on the science, don’t sensationalize and overpromise research outcomes.

Most scientists don’t have formal training in science communication. Universities and government agencies are starting to realize the importance and are working on to incorporating proper training for the next generation scientists. Some universities opened graduate program in science communication major. It’s a fast-growing field that we should all consider improving our science communication skill in the future.

References

Burns TW, O’Connor DJ, Stocklmayer SM. Science Communication: A Contemporary Definition. Public Understanding of Science. 2003;12(2):183–202.
Poliakoff E, Webb TL. What Factors Predict Scientists’ Intentions to Participate in Public Engagement of Science Activities? Science Communication. 2007;29(2):242–263.
Cooke S, Gallagher AJ, Sopinka N, Nguyen VM, Skubel R, Hammerschlag N, Boon S, Young N, Danylchuk A. Considerations for effective science communication. In: ; 2017.
Rakedzon T, Segev E, Chapnik N, Yosef R, Baram-Tsabari A. Automatic jargon identifier for scientists engaging with the public and science communication educators. PLOS ONE. 2017;12(8):e0181742.

Can your leg and arm tell a failing heart?

May 14, 2021May 7, 2021 Huan Wang, PhD

For the heart’s health condition, everything is interconnected. Other parts of the body might be reflective or instigators of a failing heart. Among all of the important issues related to cardiovascular disease, skeletal muscle is on top of that list. Conventionally, the main function of skeletal muscle is tightly related to physical capabilities. It’s only the partial facts. Skeletal muscle plays a pivotal role in supporting our physical well-being in many ways that are more than organizational. The relationship between skeletal muscle mass and cardiometabolic health starts to attract the researcher’s attention.

As we know, skeletal muscle mass decreases during the aging process, while cardiometabolic health often declines. A recently published epidemiology study investigated the relationship between skeletal muscle mass and cardiovascular disease in a group of adults (3042 people) without pre-existing cardiovascular risk in a 10-year follow-up study, ATTICA¹. After adjusting for various confounders, this study showed a significant inverse association between skeletal muscle mass and cardiovascular incidence (HR 0.06, 95% CI 0.005 to 0.78). Moreover, it showed that people in the highest skeletal muscle mass group had 81% lower risk for a cardiovascular event. The results are quite intriguing. Does decreased skeletal muscle mass contribute to poor heart health or does a failing heart cause muscle mass decrease? It’s hard to figure out the cause and effect without understanding the relationship between skeletal muscle and the heart.

Chronic heart diseases and heart failure impair muscle function². In particular, many heart diseases affect exercise performance. For certain cardiac conditions such as atherosclerotic heart disease, exercise stress test is widely used to measure heart functional capacity, and also used as a diagnostic tool to evaluate the efficacy of treatment and predict prognosis. Cardiac function affects exercise performance in many ways and reduced cardiac output response to exercise leading to skeletal muscle hypoperfusion and lactic acidosis³. The pathophysiological mechanisms impairing skeletal muscle function in heart failure are discussed in a review, shown in Fig1². In heart failure, many stimuli contribute to skeletal muscle contractility apparatus dysfunction such as systemic inflammation, TGF family members, adrenergic signaling, decreased anabolic stimuli and increased calcium shuttling/overload (Fig. 1). Skeletal muscle atrophy can be caused by biological processes such as protein degradation, impaired growth factor signaling and skeletal muscle inflammation.

Heart failure with increased systemic inflammation can trigger skeletal muscle inflammation. it’s also true the other way around: skeletal muscle injury can cause local activation of innate immune system⁴. Danger-associated molecular patterns (DAMPs) can be released from dying myocytes. DAMPs encompass diverse mediators including alarmins (HMGB1, S100A8/9/12, S100B, IL1a, HSPs), bioactive lipids, extracellular matrix fragments and nucleotides (ATP, CpG, dsRNA)⁵. The impact of local skeletal muscle immune responses has been proved both harmful and beneficial. Traditionally, a stimulated immune response (M1-like macrophages) is a sign of disease. However, distinct macrophage subsets (M2-like macrophages) help tissue regeneration in chronic skeletal muscle pathologies⁶. The relationship between skeletal muscle damage and inflammation is complicated. And how they play a role in heart diseases require more research in the future.

To go back to the original question in this blog, the answer is a yes. Yes, skeletal muscle (leg and arm muscle) can tell the basic condition of the heart. And is it good for your heart if there is more muscle mass? Maybe. The absolute muscle mass does not tell us the function of the muscle, other aspects of muscle, for example, different types of fiber may hold the key.

References

Tyrovolas S, Panagiotakos D, Georgousopoulou E, Chrysohoou C, Tousoulis D, Haro JM, Pitsavos C. Skeletal muscle mass in relation to 10 year cardiovascular disease incidence among middle aged and older adults: the ATTICA study. Journal of Epidemiology and Community Health. 2020;74(1):26 LP – 31.
Kennel PJ, Mancini DM, Schulze PC. Skeletal Muscle Changes in Chronic Cardiac Disease and Failure. Comprehensive Physiology. 2015;5(4):1947–1969.
Lunde PK, Sjaastad I, Schiøtz Thorud H-M, Sejersted OM. Skeletal muscle disorders in heart failure. Acta Physiologica Scandinavica. 2001;171(3):277–294.
Lavine KJ, Sierra OL. Skeletal muscle inflammation and atrophy in heart failure. Heart failure reviews. 2017;22(2):179–189.
Chan JK, Roth J, Oppenheim JJ, Tracey KJ, Vogl T, Feldmann M, Horwood N, Nanchahal J. Alarmins: awaiting a clinical response. The Journal of Clinical Investigation. 2012;122(8):2711–2719.
Villalta SA, Deng B, Rinaldi C, Wehling-Henricks M, Tidball JG. IFN-γ Promotes Muscle Damage in the <em>mdx</em> Mouse Model of Duchenne Muscular Dystrophy by Suppressing M2 Macrophage Activation and Inhibiting Muscle Cell Proliferation. The Journal of Immunology. 2011;187(10):5419 LP – 5428.

On the Basis of Sex: Are males more vulnerable in severity and mortality from COVID-19?

April 9, 2021April 6, 2021 Huan Wang, PhD

Fig1: Data source: The sex, Gender and Covid-19 Project. (https://globalhealth5050.org/the-sex-gender-and-covid-19-project/about-us/)

As we just passed our first anniversary of fighting COVID-19, we are in a better position than we used to be a year ago. Nationwide vaccine efforts encourage us to see the light at the end of the tunnel. However, the virus is still lurking around and always finds its way back in many unpredictable forms as it evolves rapidly. We need to stay vigilant and use what we learned from the previous years’ knowledge to guide us defend any future attacks. One pertinent piece of information we discovered is that COVID-19 attacks us unequally. People are over 65 years old and people with any underlying complications are more at risk. Another important discovery is that there is a sex difference in infection, severity, and death among women and men.

In most countries, the incidence of infection (percent of cases) is similar in both sexes. However, men consistently develop more serious symptoms and have more mortalities across age groups on a global level (Fig1). More specifically, men account for about 59% to 75% of total mortality¹. It’s indisputable that sex is an important factor when it comes to understand and combat COVID-19. Here are a couple of candidate mechanisms potentially contributing to sex-biased COVID-19 mortality.

Hormones

Many sex differences in the manifestation of disease development have long been attributed to sex hormones, particularly in the realm of immune responses. Both innate and adaptive immune responses are affected by sex-dependent factors². Males are more susceptible to infections caused by parasites, fungi, bacteria, and viruses, one of the possible determining factors is sex hormone³. More specifically, the immune-suppressive androgens reside in males and immune protective estrogens reside in females. Females might produce more antibodies and launch a stronger immune defense to infection because of estrogens, while males lack the advantage to react the same way. Female hormones, estrogens, can ameliorate the severity of influenza infections by suppressing pro-inflammatory responses in mice⁴. The anti-inflammatory activity of estrogen is potentially through the regulation of the SOCS3 and STAT3 signaling pathways, specifically to promote the progression of the anti-inflammatory process towards the IL-10-dependent pathway in macrophages⁵. Sex hormones can regulate the immune response via regulating circadian rhythm, microbial composition, and transcriptional regulation such as estrogen receptors (ERs) and peroxisome proliferator-activated receptors (PPARs)⁶.

Fig2: Potential mechanisms of male bias of COVID-19 mortality7.

Sex chromosomes

One of the fundamental differences between men and women is the X and Y sex chromosomes. Females have two X chromosomes with a functional one and an inactive one to maintain the balance of chromosomal X gene dosage, while males only have one functional X chromosome and one Y chromosome to maintain the identity of sex-specific effects and testis development. This evolutional advantage in females provides a “back-up” plan in case of a “disease gene” on X chromosome inherited from either the maternal or paternal side. Some genes can escape from X chromosomal inactivation and consequently express higher levels. The gene encoding a receptor that is responsible for SAS-CoV-2 virus cellular entry is called ACE2. ACE2 locates at X chromosome and is potentially a target for ineffective chromosome inactivation, and which could cause a female-biased increased level of ACE2 expression⁷. A higher level of ACE2 in females promotes viral clearance. On the contrary, a lower level of ACE2 causes dysregulated inflammation, increased cardiovascular comorbidities, increased risk of respiratory failure in males⁷ (Fig2). Other inflammatory response-related genes on the X chromosome include pattern recognition receptors such as toll-like receptor 7 (TLR7), TLR8, interleukin-1 receptor-associated genes, and NFKB essential modulator genes⁸. Additionally, it has been shown that TLR3, TLR7, and TLR9 are female-biased while TLR2 and TLR4 are male-biased. These differences potentially reveal why males and females respond to infection differently^7,8. The research on understanding sex dimorphisms in immunity is critical to help us fight COVID-19 more effectively.

In conclusion, strong evidence shows that COVID-19 affects men and women unequally. Aside from socio-economic, lifestyle and environmental differences, biology plays an important role in male-biased COVID-19 severity and mortality. To understand and combat infection more precisely, we need to consider sex as a biological variable and develop therapeutic strategies for men and women respectively.

References

Griffith DM, Sharma G, Holliday CS, Enyia OK, Valliere M, Semlow AR, Stewart EC, Blumenthal RS. Men and COVID-19: A Biopsychosocial Approach to Understanding Sex Differences in Mortality and Recommendations for Practice and Policy Interventions. Preventing chronic disease. 2020;17:E63.
Markle JG, Fish EN. SeXX matters in immunity. Trends in Immunology. 2014;35(3):97–104.
Klein SL. The effects of hormones on sex differences in infection: from genes to behavior. Neuroscience & Biobehavioral Reviews. 2000;24(6):627–638.
Robinson DP, Lorenzo ME, Jian W, Klein SL. Elevated 17β-Estradiol Protects Females from Influenza A Virus Pathogenesis by Suppressing Inflammatory Responses. PLOS Pathogens. 2011;7(7):e1002149.
Villa A, Rizzi N, Vegeto E, Ciana P, Maggi A. Estrogen accelerates the resolution of inflammation in macrophagic cells. Scientific Reports. 2015;5(1):15224.
Taneja V. Sex Hormones Determine Immune Response. Frontiers in immunology. 2018;9:1931.
Bienvenu LA, Noonan J, Wang X, Peter K. Higher mortality of COVID-19 in males: sex differences in immune response and cardiovascular comorbidities. Cardiovascular Research. 2020;116(14):2197–2206.
Pradhan A, Olsson P-E. Sex differences in severity and mortality from COVID-19: are males more vulnerable? Biology of Sex Differences. 2020;11(1):53.