Urban Decay: Mushrooms on a Dead Tree

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

Dark orange ear-shaped mushrooms recently appeared on a small sidewalk tree in my neighborhood. Failing to grow, the tree has now missed its blooming cycle for two consecutive summers. This summer’s weather, in New York City, has been marked by heat and high humidity. Higher-than-average precipitation has even resulted in flash flooding. Sudden appearance of mushrooms  is an indication of rot and decay  inside the tree.  While heavy rains combined with extended periods of high heat and humidity can trigger rapid mushroom growth, and although their appearance seems spontaneous, an internal fungal network has been growing inside the tree for several months to years.

Mushrooms are the spore forming fruit of  a larger hidden body of thread-like mycelium. In most instances mushrooms decompose dead wood,  indicating that the tree is dead. By the time you see mushrooms, the tree has been rotting from the inside out.  As a result, trees covered in mushrooms are structurally compromised and at risk of falling. Public trees in NYC are governed by the  NYC Department of Park and Recreation  and dead trees should be reported for removal using the interactive NYC Tree Map or by calling 311.

The “root-cause” of why the tree died  is not certain but there are some clues…

Diagram of zelkova sidewalk tree showing trunk mushrooms, inner wood decay, and damaged roots

Japanese Zelkova

Using the Park Service’s map, I was able to identify the tree as a Japanese Zelkova (Zelkova serrata), also  known as  Keyaki or Keaki. Native to Japan and other parts of Asia, like Korea and Taiwan, Japanese Zelkova were introduced to America in 1862 Due to their ability to grow in acidic, alkaline, moist, and arid soil they have been considered good for street planting or what is known as urban greening. Japanese Zelkova are reportedly effective in purifying urban air due to their canopy of leaves which absorb carbon dioxide (CO2) and capture  particulate matter (black carbon and dust) present in ambient and traffic related air pollution. Trees, in general, function as biofilters, mitigating vehicular emissions and improving air quality. The Zelkova in my neighborhood has been standing since at least 2017 and although not a large trees, it is reported as having annually intercepted 346 gallons of storm water and removed one pound of air pollutants.

Zelkova’s are deciduous hardwood trees that prefer full sun and are capable of surviving urban environmental stress, such as high temperatures, low humidity, drought, and soil limitation. In cities, trees often have limited space for their roots and may experience water stress. Although one of many trees on my block, the Zelkova enjoyed unincumbered sunlight being a good distance from others. Relatively young, this Zelkova would not have undergone considerable pruning, where incorrect pruning could have hindered spring foliage or trunk damage could allow fungal spores to enter. Deciduous trees shed their leaves annually, during autumn in preparation for winter. While freezing weather, like what occurred this winter in NYC this year, can cause dieback in which branches fail to produce foliage, the previous year was comparatively mild yet the tree produced not one leaf. Neither budding nor blooming, the Zelkova remained relatively small and leafless for two consecutive summers despite previous normal flourishing. Trees that have stalled in overall growth and fail to produce foliage likely have incurred long-term nutrient deficiencies from water conductivity failure indicating a problem with the roots.

Root of the Matter

Roots play a significant role in water uptake which affects photosynthesis and carbon dioxide (CO2) absorption. Normal Zelkova root hydraulics efficiently balances water uptake  with carbon gain which affects overall growth. Root girdling can occur in trees planted in narrow sidewalk cutouts, where the roots eventually run out of room and start circling the trunk below the surface. This causes vascular compression and failure, as both the trunk and roots expand in diameter. Compression deforms internal xylem tissue and phloem bark gradually choking off water (hydraulic failure) and nutrient absorption (nutrient starvation). The result is stunted foliage and branch death. Xylem are the specialized transport tissue that moves water and dissolved minerals upward from the roots, comprising what we know as wood. Phloem is the living inner bark of the tree that  carries carbohydrates and sugars made in the leaves to the rest of the tree. Therefore, uptake and transport throughout the tree would be compromised. Deep planting, compacted soil, and salt injury could also contribute to root problems and canopy loss.

Wood Ear Fungi

Mushrooms are heterotrophic eukaryotic organisms. Heterotrophs cannot make their own food and must get energy from other plants, animals or organic matter. Therefore, mushrooms form various types of relationships with the trees they grow in order to derive the nutrients they need. Saprotrophic mushrooms feed on dying trees and deadwood, secreting digestive enzymes that decompose wood into cellulose (a polysaccharide) and lignans (polyphenols). Mycorrhizal mushrooms form mutualistic relationships, providing water and minerals to trees while the tree in turn provides sugars. Parasitic mushrooms infect and feed on healthy living trees, harming and potentially killing them.

The mushrooms growing on the tree are orange ear-shaped and clustered with some having turned black. They are likely Wood Ear fungi (Auricularia sp.), which darken as they dry and age and are known to grow on dead hardwood trees making them saprotrophs. The location of the mushrooms can also be informative, with mushrooms at the base and roots of a tree indicative of root or butt rot, while  mushrooms on the trunk informs of heartwood decay (heartwood is the central wood of the tree). Mushrooms on branches are not always a sign of disease or death as it can be common and may only require pruning of the affected branch. The mushrooms on the Zelkova on my sidewalk are located high on the trunk of the tree, near the start of the branches, with a few extending upward. This is another clue that points to vascular/root dysfunction, also suggesting that the development of fungi/mushrooms are a symptom of an underlying problem and not the original cause of death. Mushrooms emerging around the juncture of major branches also indicates significant internal decay as in most cases fungi decompose wood tissue.

Mushrooms can also be categorized as edible or inedible. Various species of Wood Ear fungi are used as a food ingredient, particularly in Asian cuisines. Although belonging to different families, other saprotrophic mushrooms that grow on hardwood trees like Shiitake, Turkey tail, Oyster, and Reishi are also edible and said to have medicinal properties. While these mushrooms can be nutritious and have beneficial properties (anti-inflammatory/antioxidant, lipid-lowering, and antitumor), scavenging urban mushrooms from a sidewalk tree is not recommended. Cultivated mushrooms that have been grown in a controlled environment avoids contamination that can occur from traffic-related pollution and other side-walk city activity.

City Contamination

Since mushrooms play a role in environmental element cycling, transforming organic and inorganic matter into minerals, they can absorb and accumulate metals and pollutants from the surrounding microenvironment.  Mushrooms can contain an excess amount of heavy metals like cadmium (Cd), lead (Pb), arsenic (As), and mercury (Hg) due to the abundant presence of metallothionein in mushrooms. Metallothionein binds heavy metals causing them to accumulate in mushrooms. Accumulation varies by species and location, and cultivated mushrooms show lower accumulation of toxic metals than those associated with urban sites. While fungal species growing on wood generally contain lower concentrations of metals than fungi growing in soil, the main uptake route of these toxic metals is by means of absorption from soil through the vascular/root system.

Soil around city street trees were found to have increased salinity and alkalinity which affected micronutrients. Road salting is primarily responsible for higher amounts of nutrients like sodium (Na), Chloride (Cl), Calcium (Ca), Zinc (Zn), and Copper (Cu) in sidewalk trees, which were also found to have higher pH and lower potassium (K) and magnesium (Mg). Consequently, increased soil salinity can also lead to poorer foliage (leaf production not folate). Other factors influencing nutrient uptake from soil are the pH, carbon to nitrogen ratio, moisture, soil temperature, climate, and other street-associated factors. Urban soil can also have poor aeration due to compaction and low organic matter content which normally buffers the absorption of traffic-related pollutants into soil. Without leave and ground level organic matter to mitigate pollution, increased deposition of heavy metals can occur. Sidewalk soil has been found to be contaminated with cadmium, lead, zinc, and copper with their deposition also influenced by distance from the road, proximity to a highway, parking area, and density of traffic. Even at low concentration, chronic deposition can lead to gradual accumulation in urban environments. These factors can impact soil quality, affecting root and tree vitality and accumulation in subsequent mushroom growth.

While zinc and copper are essential trace elements that are safe and necessary at low-levels, cadmium and lead are non-essential metals with no known biological benefits in humans. Toxic metals have been associated with cardiovascular and respiratory diseases, neurological disorders, chronic inflammation, and cancers. Other organic roadside soil contaminants include PAHs (polycyclic aromatic hydrocarbons) and TPH (total petroleum hydrocarbons). PAHs can originate from pyrogenic (burning coal, oil, gas, wood, or tobacco) or petrogenic (petroleum) sources, and consist of  fused benzene ring structures that can be highly toxic. Other petroleum hydrocarbons classified as TPH include aliphatic (chains/non aromatic rings) compounds. Urban environments are notoriously affected by pollution from traffic and industrial activities which can have adverse consequences for both urban ecosystems and human health. Particularly, bioaccumulation from soil to trees and mushrooms to humans can intensify the bioavailability of harmful substances through diet. So, think twice and avoid snacking on roadside mushrooms even if they are growing freely on a city tree.

Connecting the Dots

Ultimately, the Wood Ear mushrooms growing on the Japanese Zelkova are less a cause of its decline than a visible indication of a much longer process of decay occurring beneath the bark and below the sidewalk. Although the exact root-cause of its death is uncertain, restricted roots, compacted and contaminated soil, road salt, and other urban stresses may have impaired the trees ability to transport water and nutrients, weakening it over-time. By the time the orange, ear-shaped mushrooms appeared, the tree had already failed to produce leaves for two consecutive summers, suggesting that its internal systems had been compromised for some time. This summer’s combination of heavy rainfall, high humidity, and extreme heat likely provided ideal conditions for the rapid growth of the fungi, making an existing problem suddenly visible. The mushrooms therefore are not necessarily what killed the tree, but a sign that the tree was already dead or dying and that its remaining wood is now being returned to the environment. both trees and mushrooms are key components of urban ecosystems that act simultaneously as recipients and mitigators of environmental pollution. displayed on my block, a dead tree and the mushrooms growing on it acting as nature’s recycling system, turning dead things into new life.

References

  • Manici, L. M., De Meo, I., Saccà, M. L., Ceotto, E., Caputo, F., & Paletto, A. (2023). The relationship between tree species and wood colonising fungi and fungal interactions influences wood degradation. Ecological Indicators, 151, 110312. https://doi.org/10.1016/j.ecolind.2023.110312
  • Qin, G., Liu, J., Zou, K., et al. (2024). Analysis of heavy metal characteristics and health risks of edible mushrooms in the mid-western region of China. Scientific Reports, 14, 26960. https://doi.org/10.1038/s41598-024-78091-1
  • Schlecht, M. T., & Säumel, I. (2015). Wild growing mushrooms for the edible city? Cadmium and lead content in edible mushrooms harvested within the urban agglomeration of Berlin, Germany. Environmental Pollution, 204, 298–305. https://doi.org/10.1016/j.envpol.2015.05.018
  • Singh, R., Chavan, S. B., Tomar, A., et al. (2025). Species variation in air pollution tolerance, performance, and dust retention of urban roadside trees: Implications for urban greening and green corridor planning. Air Quality, Atmosphere & Health, 18, 3311–3327. https://doi.org/10.1007/s11869-025-01841-1
  • Taneda, & Ikeda. (2021).Hydraulic architecture with high root-resistance fraction contributes to efficient carbon gain of plants in temperate habitats. American Journal of Botany, 108(10), 1932–1945. https://doi.org/10.1002/ajb2.1753
  • Tedoldi, D., Charafeddine, R., Branchu, P., Thomas, E., & Gromaire, M.-C. (2021). Intra- and inter-site variability of soil contamination in road shoulders—Implications for maintenance operations. Science of The Total Environment, 769, 144862. https://doi.org/10.1016/j.scitotenv.2020.144862
  • Wang, M., & Zhang, H. (2018). Accumulation of heavy metals in roadside soil in urban area and the related impacting factors. International Journal of Environmental Research and Public Health, 15(6), 1064. https://doi.org/10.3390/ijerph15061064
  • Taleghani, A., Emami, S. A., & Tayarani-Najaran, Z. (2020). Artemisia: A promising plant for the treatment of cancer. Bioorganic & Medicinal Chemistry, 28(1), 115180. https://doi.org/10.1016/j.bmc.2019.115180
  • Raymond Chang, Functional Properties of Edible Mushrooms, Nutrition Reviews, Volume 54, Issue 11, November 1996, Pages S91–S93, https://doi.org/10.1111/j.1753-4887.1996.tb03825.x
  • Malvandi H, Parsan H, Gharaei A, Fallahinejad S. (2026). Integrated Assessment of Heavy Metal Accumulation in Urban Trees and Soils and Associated Non-carcinogenic Health Risks in Sabzevar, Iran. Bull Environ Contam Toxicol. Aug 11;117(2):42. doi: 10.1007/s00128-026-04316-w. PMID: 42579006.

Why Some People Notice Their Skin Lightens After Major Weight Loss: The Strange Connection Between Fat, Inflammation, and Melanin

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

There’s a phenomenon that some people notice after major weight loss, but almost never have a scientific reasoning for it. Someone loses a large amount of body fat — 50 pounds, 100 pounds, sometimes more — and over time they notice something unexpected: Their complexion looks lighter. Not pale exactly, and not sickly, but fairer. Sometimes the change is subtle. Sometimes friends or family notice it before they do.

The phenomenon is largely anecdotal, among melanated people especially, stories about skin tone shifting after significant fat loss are surprisingly common. Usually, the explanation gets dismissed as lighting, reduced sun exposure, anemia, or simple perception. However, over the past two decades, researchers studying obesity, adipose tissue biology, inflammation, and pigmentation have uncovered several biological connections that make this observation far less mysterious than it first appears. What began as research into obesity-related inflammation has evolved into a broader understanding of how adipose tissue communicates with the immune system, oxidative stress pathways, and even melanogenesis — the biological process responsible for melanin production.

Read more below to find out why losing weight may cause your skin to lighten and how scientist are exploring the use of extracellular vesicles from fat cells to develop cosmetic therapeutics to combat hyperpigmentation and skin aging.

The Link Between Fat Tissue and Pigmentation

Adipose tissue is not “inactive” fat. For most of medical history, adipose tissue (fat), was regarded simply as excess energy storage, resulting from over consumption of food (dietary fats, sugars, and excess calories). Overtime, researchers began studying obesity at the molecular level. Now, adipose tissue is recognized  as an active endocrine and immunological organ.

In the endocrine and immune systems, fat tissue  produces hormones, cytokines, inflammatory mediators, and signaling molecules capable of influencing nearly every major body system. The more fat you gain, the larger adipose tissue becomes, particularly visceral fat — the fat surrounding organs. Excessive adipose tissue becomes more metabolically active and more inflammatory, which explains why obesity is strongly associated with chronic low-grade systemic inflammation, oxidative stress, insulin resistance, altered hormone signaling, and immune dysfunction.

In particular, inflammation and oxidative stress directly influence pigmentation.

Melanin is not just a pigment. For a long time, melanin was thought to exist primarily in specialized pigment-producing cells called melanocytes. These cells are found mainly in the skin, hair follicles, and eyes, and melanin is best known for determining skin and hair color.  However, biologically, melanin also possesses potent antioxidant and anti-inflammatory properties. Interestingly, these properties play an important role in the relationship between fat and melanin production.

In 2010, researchers proposed that adipose tissue itself may participate in melanogenesis. In their review Melanin and melanogenesis in adipose tissue: possible mechanisms for abating oxidative stress and inflammation?, Page, Chandhoke, and Baranova examined evidence showing that adipose tissue expresses several genes related to melanogenesis and may produce melanin in response to metabolic stress. Researchers found that:

  • Obesity is strongly associated with chronic low-grade inflammation
  • Obesity is associated with increased oxidative stress
  • Visceral adipose tissue from obese individuals contained more melanin compared to lean individuals

These finding led the researchers to hypothesize that melanin may function as a protective antioxidant defense mechanism inside adipose tissue . In other words, the body may increase melanogenesis in fat tissue as a compensatory response to chronic metabolic stress.

This theory may help explain why some individuals with obesity develop increased pigmentation or darker complexions over time — particularly when obesity is accompanied by systemic inflammation and insulin resistance.

Leptin, the Brain, and Melanin

Melanin is also expressed in certain regions of the central nervous system (brain). The Hypothalamus produces a neuropeptide known as melanin-concentrating hormone (MCH) which is important for regulating feeding behavior and energy balance. Interestingly, researchers discovered that adipocytes (fat cells that make up adipose tissue) also possess receptors for MCH.

In adipose tissue,  MCH plays a role in the production and function of Leptin. One of the most important hormones produced by adipose tissue, leptin is a hormone that regulates appetite and satiety. This action is mediated by MCH through the hypothalamus.

Leptin also has major immune and inflammatory functions.  Increased body fat raises leptin levels, and high leptin level promote inflammatory cytokine production. In turn, inflammatory cytokines can further increase leptin production. This creates a self-perpetuating inflammatory feedback loop frequently seen in obesity.

These findings suggest that pathways involved in pigmentation, appetite regulation, neuroendocrine signaling, and adipose biology may all intersect.The relationship between adipose tissue and melanin associated pigmentation therefore appears to involve, oxidative stress, inflammation, endocrine activity, and melanogenic gene expression.

Inflammation, Insulin Resistance, and Hyperpigmentation

Excess fat creates a chemical microenvironment that encourages pigmentation. As we saw, fat tissue produces inflammatory cytokines. These cytokines can alter insulin signaling leading to insulin resistance and increase metabolic stress. Metabolic stress increases oxidative stress and more inflammation, and all of these systems intersect with melanogenesis. Lets  break down how:

One of the clearest clinical examples connecting obesity and pigmentation is a condition called acanthosis nigricans.

Acanthosis nigricans is a hyperpigmentation disorder that  commonly appears in individuals with obesity, insulin resistance, Type 2 diabetes, and metabolic syndrome. People with the condition develop thick, darkened, velvety patches of skin – usually localized around the neck, armpits, groin, and body folds, unlike generalized skin darkening. However, Acanthosis nigrican demonstrates an important principle: Metabolic dysfunction and chronic inflammation can visibly influence pigment production and skin cell growth.

Hyperinsulinemia associated with insulin resistance stimulates pathways that increase keratinocyte proliferation and melanocyte activity. Simultaneously, oxidative stress and inflammatory cytokines can further amplify melanogenesis. As obesity is often responsible for insulin resistance and Type 2 Diabetes, excess fat may thereby create a biological environment that promotes increased pigmentation signaling throughout the body.

Why Weight Loss May Ligthen Complexion

Although the scientific literature has not definitively proven that fat loss causes lighter skin tone, several mechanisms make the observation biologically plausible.

If obesity increases systemic inflammation, oxidative stress, insulin resistance, leptin, and potentially compensatory melanin production, then major fat loss may reduce those same signals. Weight loss alters systemic inflammation, oxidative stress, and hormonal and cytokine signaling.

As inflammation and oxidative stress are known stimulators of melanogenesis, reducing these signals may lowers the body’s overall demand for melanin production. Also, since obesity increases reactive oxygen species (ROS) production, and melanin acts as a scavenger of ROS, reducing adipose tissue could theoretically reduce oxidative stress and consequentially, compensatory melanogenesis. Additionally, as leptin, insulin, and adipose cytokine secretion by fat issue intersects with inflammatory and melanogenic pathways, changes in body fat may indirectly influence pigmentation.

In simpler terms:

Inflammatory burden goes down, insulin sensitivity improves, oxidative stress decreases, circulating leptin is lowered, and there is overall less chronic metabolic stress. Less metabolic stress may mean less need for melanin-related protective activity.

If melanogenesis is functioning partly as a protective response to oxidative and inflammatory stress, then reducing the underlying stress environment could theoretically reduce melanogenic activity as well. This may be enough to produce visible changes in complexion for some people following dramatic weight loss. Although this change may not occur overnight or as dramatically in every individual, it is possible.

A New Frontier: Adipose Stem Cellular Vesicles

Illustration of an adipose stem cell with nucleus releasing molecular messages, showing intracellular packing and extracellular travel of molecules
Illustration showing how an adipose stem cell communicates by releasing molecular messages.

While dysfunctional adipose tissue may contribute to inflammatory stress, scientists are now discovering that biological nanoparticles released from adipose stem cells may possess the opposite effect.

These particles are called extracellular vesicles, lipid-bound particles releases by cells that contain microRNA’s, proteins, and lipids. EVs act as communication systems between tissues and organs and help regulate cellular homeostasis. Interestingly, small EVs (~200 nm in diameter) often perform functions that differ from — or even oppose — those of their parent cells.

In 2025, emerging research on adipose-derived small extracellular vesicles investigated their use in cosmetic therapeutics. Researched assessed adipose stem cell small EVs (ASC-sEVs) as delivery systems for natural antioxidant compounds. Remarkably, researchers discovered that  ASC-sEVs demonstrated anti-melanogenic effects in melanocyte cells.

By themselves,  the vesicles reduced melanin production, but when loaded with antioxidant compounds like resveratrol and arbutin,  anti-melanogenic effects became significantly stronger. Likely, due to the vesicles’ ability to improve skin penetration of the antioxidant compounds. Additionally, the vesicles enhanced compound stability, bioavailability, and intracellular delivery while requiring lower therapeutic concentrations than the antioxidants alone. Importantly, the treatments were not cytotoxic.

This introduces a fascinating paradox: while obesity-associated adipose tissue may contribute to inflammatory melanogenic signaling, extracellular vesicles derived from adipose stem cells may simultaneously possess regulatory and anti-pigmentary functions capable of restoring balance.

Timeline of the Science Connecting Adipose Tissue, Inflammation, and Melanin

Pre-2000s            2000                Mid-2000s            2008–2011              2010s                 2021                   2025                  Present
     ●──────────────────●────────────────────●────────────────────●────────────────────●────────────────────●────────────────────●────────────────────●
 Passive fat        MCH receptors         Obesity viewed       Melanin found         Insulin resistance   Obesity reframed     ASC-sEVs shown      Integrated model
 storage model      discovered in         as inflammatory      in adipose tissue     linked to            as neuroimmune       to reduce           emerging:
                    adipocytes            condition            + melanogenesis       hyperpigmentation    endocrine disorder   melanogenesis       fat, inflammation,
                                                                 genes identified                                                   + enhance           oxidative stress,
                                                                                                                               antioxidant delivery pigmentation
                                                                                                                                                       linked together
                     ↓                     ↓                    ↓                     ↓                     ↓                    ↓                    ↓
               Fat tissue            Cytokines, ROS,     Melanin proposed      Acanthosis            Leptin linked      Adipose stem-cell     Weight loss may
               linked to             leptin, and         as antioxidant        nigricans shows       to inflammation,   EVs explored as       reduce systemic
               neuroendocrine        insulin resistance  defense mechanism     metabolism can        immunity, and      regenerative          melanogenic
               signaling             become central      against oxidative     alter pigmentation    metabolic          therapeutics          signaling through
                                                            stress                                      homeostasis                             lower inflammation

Conclusion

The relationship between body fat and skin pigmentation is far more biologically complex than previously understood.

Emerging evidence suggests that obesity-associated inflammation, oxidative stress, insulin resistance, and endocrine signaling may all influence melanogenesis both locally and systemically.

This may help explain why some individuals notice skin lightening after major fat loss: reduced adipose burden may decrease inflammatory and oxidative signals that promote compensatory pigmentation activity.

At the same time, modern research is revealing a fascinating duality within adipose biology itself. While dysfunctional adipose tissue can contribute to chronic inflammation, adipose-derived extracellular vesicles may possess powerful regenerative and anti-melanogenic properties capable of restoring cellular balance.

What once seemed like a cosmetic anecdote may ultimately become part of a much broader scientific story connecting metabolism, pigmentation, inflammation, and regenerative medicine.

References

Bradley, R. L., Kokkotou, E. G., Maratos-Flier, E., & Cheatham, B. (2000). Melanin-concentrating hormone regulates leptin synthesis and secretion in rat adipocytes. Diabetes, 49(7), 1073–1077. https://doi.org/10.2337/diabetes.49.7.1073

Page, S., Chandhoke, V., & Baranova, A. (2011). Melanin and melanogenesis in adipose tissue: Possible mechanisms for abating oxidative stress and inflammation? Obesity Reviews, 12(5), e21–e31. https://doi.org/10.1111/j.1467-789X.2010.00773.x

Procaccini, C., La Rocca, C., Carbone, F., & Matarese, G. (2021). Leptin and obesity: Role and clinical implication. Frontiers in Endocrinology, 12, 585887. https://doi.org/10.3389/fendo.2021.585887

Vo, N., Vu, D. M., Tran, N. H. B., Nguyen, D. D. N., Phung, P. M., Nguyen, H. N., & Tu, L. N. (2025). Synergistic anti-aging effects of adipose-derived stem cell extracellular vesicles loaded with natural compounds. Journal of Cosmetic Dermatology, 24(2), e70021. https://doi.org/10.1111/jocd.70021

Vampirism or Rabies

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

If you wake up to a bat in your bedroom its very likely that you will turn into a vampire.

A vampire is described as an insomniac creature – awake at night – with a fear of water. Most notably holy water, but any running water is proposed to kill a vampire or prevent the dead from rising as one.

You might not be aware that you were bitten, because the bite might be smaller than you expect and you probably would not feel anything at all, at first!

However, within weeks or over the course of three months you may start to experience anxiety and confusion. It could just be paranoia, and perhaps you tell yourself, “I worry too much”, but then delirium and hallucinations set in. You start to act strangely, staying up all night and recoiling at the sight and sound of water.  Now you are turning, now it’s too late, because by this time, when you start to experience these symptoms there’s no cure for this sort of vampire disease.

Unfortunately for you, you will not live forever, but will suffer a most fatal demise, because there is no such thing as vampires. You have rabies!

Rabies is a viral disease, of the family Rhabdoviridae and genus Lyssavirus. It is transmitted from animals to humans, usually through the bite or scratch from a bat who is the leading cause of rabies in the United States, but also raccoons, foxes, skunks, and more, according to the CDC.

Rabies virus is insidious, creeping into your central nervous system by traveling up the axons of neurons to the spinal cord and into your brain where it incubates for weeks or months. There it will cause inflammation of your brain while it multiplies – you’ll start to experience headaches, irritability, malaise, and sensitivity to sound and light, but don’t pull the blinds yet.  The virus spreads back into your body where it can be found in your saliva. Please don’t bite me, I’m only trying to warn you.  If you find it impossible to swallow water, know that your time is short. This soon will turn into paralysis, and you won’t be able to control your bodily functions as you slip into a coma.

Are you scared yet? Well don’t be. If you encounter a bat or any rabid animal, and could have been bitten, wash your wound with soap and water, and get to the doctor immediately for treatment. Anti-rabies serums, anti-tetanus procedures, and rabies vaccines can be administered to prevent the development of the disease. This must be done before the onset of clinical symptoms, as the best course of action is prevention, there is no effective treatment once the infection is established.

COVID-19 Risk Predicted by Blood Type

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

Your blood type might put you at greater risk for COVID-19, according to a paper published this month in the Blood Advances by researchers from Harvard. Inspired by recent genome-wide association studies which found the locus responsible for blood type expression to be among the most significant genetic predictors of SARS-COV-2 infection, they found that SARS-COV-2, the coronavirus responsible for COVID-19 preferentially binds blood group A, likely making people with this blood type more susceptible to infection.

There are several blood groups found in humans. The basic blood groups are denoted ABO(H) for the carbohydrate chains A, B, AB, and O, with H representing the “Bombay phenotype” which can be present or absent. In addition there is the rhesus factor, which plays a role in blood transfusion compatibility and can be negative (-) or positive (+), making one either A-, A+, B-, B+, and so on.

I tested my blood type with these cards in a fun lab activity after donating blood for a study

The reason why your blood type might influence your risk for infection by the virus is because, the receptor-binding domain of SARS-COV-2 shares genomic sequence similarity with an ancient lectin family called galectins that are known to bind blood group antigens.

Galectins are proteins that bind carbohydrates (string of sugars) and exhibit a high affinity (binding capacity) for the blood group antigens.  Genomic sequencing revealed similarities between the receptor binding domain of SARS-COV-2 and human galectin, making the virus capable of recognizing blood group antigens in humans. The receptor binding domain is part of the spike protein on the surface of the virus that is responsible for infection, and researchers have determined that it also displays a preference for blood group A.

Importantly, the virus does not bind well to blood group A antigens expressed on the red blood cells (RBC’s) in the blood, which may be very fortuitous, as this might have lead to hemolysis (red blood cell destruction) or greater morbidity and mortality. However, experiments revealed that the virus instead binds preferentially to organ tissues expressing a variation of the blood group A sugar. Specifically, SARS-COV-2 binds to epithelial cells in the respiratory tract. This can be understood in the adverse respiratory signs and symptoms associated with pulmonary infection by the virus, such as, cough, shortness of breath, pneumonia, and overall damage to the lungs.

The reason for this difference in affinity is that RBC’s express type II (B1-4) blood group antigens, which differ slightly in structure to the blood group antigens in the respiratory epithelium. Respiratory epithelial cells in the airways of the lungs express type I (B1-3) blood group antigens. The receptor binding domain of SARS-COV-2 binds the type I structure better than the type II structure found in RBC’s.  Interestingly, this was also reported to be the case with SARS-COV-1, the Coronavirus responsible for the SARS (Severe Acute Respiratory Syndrome) outbreak in the early 2000’s. SAR-COV-1 and SAR-COV-2 share over 85% genomic similarity, so it’s not surprising that the receptor binding domain of their spike proteins would both preferentially bind the same blood type.

Interesting facts about blood groups

  • H deficiency is rare; most people have it.
  • O+ is the most common blood type and is found most frequently in Black/African-American and Latinx populations.
  • Caucasians are just as likely to be blood type O+ as they are A+, the second most common blood type in the United States.  
  • AB- followed by B- then AB+ and B+ are the rarest blood types, respectively.

The most significant finding was that SARS-COV-2 recognizes and binds more readily to blood group A antigens, when compared to the other blood groups. Therefore, blood type A is a strong predictor for increased susceptibility to infection by coronavirus SARS-COV-2. As for morbidity and mortality, blood group A has not been associated with increased risk of morbidity or mortality, and the major risks factors for severe disease or death from COVID-19 are age over 65, Caucasian race, and male gender. Though, researchers debate whether blood type A also contributes to the disease severity of COVID-19, it likely plays a role in the progression of the disease.

It is important to note, that while blood type A might increase your risk of contracting SARS-COV-2, there is no blood type that confers protection against the virus and COVID-19. Therefore, it is still necessary to follow all preventative measures such as wearing a mask, social distancing, and hand-washing. Vaccination is also effective at decreasing the risk of severe illness or death from COVID-19 and may also protect against infection in the first place.

References

  1. Shang-Chuen Wu, Connie M. Arthur, Jianmei Wang, Hans Verkerke, Cassandra D. Josephson, Daniel Kalman, John D. Roback, Richard D. Cummings, Sean R. Stowell; The SARS-CoV-2 receptor-binding domain preferentially recognizes blood group A. Blood Adv 2021; 5 (5): 1305–1309. doi: https://doi.org/10.1182/bloodadvances.2020003259
  2. Ramo A, Mehrotra H, Onwubiko I, et al. Correlation between ABO blood groups and disease severity and mortality in hospitalized COVID-19 patients. Presented at: 62nd American Society of Hematology (ASH) Annual Meeting and Exposition; December 5-8, 2020. Abstract 104.

Racial Disparities in Cell Culture

~ Dr. Stacia Nicholson, PhD ~ 1 Comment

Racial disparity exists in various diseases that occur in human. In particular, the incidence and severity of Prostate Cancer is greater in black men than in white men in the United States. There are intrinsic biological differences that account for the differences in disease development and progression, but these differences are under-studied. Socially, cultural beliefs, as well as, inherent biases and systemic racism contribute to disparities in diagnosis, treatment, and prognosis of prostate cancer in black men on the macrolevel. However, at the biomedical and microlevel, an under appreciation or lack of awareness of the significance of ethnic and racial biological differences has resulted in inadequate diversity in bio-specimens and cell-line models in in vitro research.

Precision medicine is a growing field of interest in the treatment of diseases like cancer, where medicine and therapeutic intervention is tailored to the individuals genotype. However, with that, it is necessary to examine how ethnicity and race influence pathogenesis and progression of a disease, as well as, responsiveness to therapeutic intervention. Currently, the majority of biological samples that are collected from patients are collected from those who are classified as white or of European ancestry. Continue reading →

Reinfected & Asymptomatic? That’s a Negative! Coronavirus Case Report and Why Words Matter

~ Dr. Stacia Nicholson, PhD ~ 1 Comment

By now we are all aware that we are in the midst of a “global public health emergency” due to a novel coronavirus known as SARS-CoV-2, which causes the disease COVID-19. The “novelty” of this virus only refers to the fact that it is new; this is not a romantic title for a deadly virus. In all seriousness, the virus that arose late last year in Wuhan, China has now spread to over 25 other countries and has killed, on average, at least 2.3% of the > 90,000 people it has infected (fatality rate increases in older populations; 8 to 14.8 %). As a result scientists and doctors are racing to catch pace with the virus, not only to develop a vaccine, but to characterize how this coronavirus behaves in its victims.

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Recently, the media has caught wind of some of the reports coming out of the laboratories and clinics, and in what appears to be a hast of misunderstanding have produce more fear and misinformation. The news media has reported that some people who had COVID-19 were re-infected with SARS-CoV-2 after recovering and being discharged from the hospital. Given that there is no precise treatment or approved vaccine, the idea that one could contract the virus again, after just having it, portends that SAR-CoV-2 is insidious; and has sent many people into a panic as its characterizes the virus as being monsterous and unstoppable. It would also mean that SARS-Cov-2 is operating beyond the conventions of virology and immunology.

However, that is not the case and here is why: Continue reading →

Laundry Detergent & Allergies

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

 

A recent study published in 2018 showed that laundry detergent and detergent residue left behind after rinsing may be responsible for the increase in asthma and allergy in humans. Synthetic laundry detergents contain numerous ingredients that are irritants and sensitizers. Surfactants, the substance responsible for creating suds in the wash and bleaches can irritate the skin and respiratory airways leading to the lungs, while fragrances and enzymes can induce sensitization. Researchers found that anionic surfactants disrupt the lining of the airways (bronchial mucosal epithelial barrier) leading to the lungs. Continue reading →

Taurine: From Bull Urine to Disease Treatment

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

bullThere is a common misconception that the popular energy drink RedBull contains urine or sperm from bulls, because it contains taurine. The myth stems from the fact that taurine was originally isolated from Ox bile (bulls and oxen are male cows) in the 1800’s. While initially identified in the bile (produced by the liver) of male cows, taurine is widely found in almost every organ in mammals. Taurine is chemically synthesized and used as an ingredient in infant formula, energy drinks, nutritional supplements, and pet food. Most recently it has been identified for its therapeutic value in the treatment of congestive heart failure and other cardiovascular diseases. It is currently being studied for its further use in the treatment of  other diseases, in particular those relating to  the nervous system, muscles, and mitochondrial disorders.

What is Taurine?

Continue reading →

Genetically Engineered Heme in Vegan Meat

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

Three Masters of Science graduates were overheard talking about the impossible burger— if you haven’t heard about it, it is a vegan-meat substitute produced by Impossible Foods Inc. which palatably mimics an actual ground-beef burger. The one was telling the others, that the burger was not only delicious and filing, but that it smelled and tasted like real beef. When questioned as to what gave it the beef-like sensation, she answered heme, but was unsure of the source of the heme. This was puzzling because most people are familiar with heme being a component of animal blood, and the idea that heme could be vegan or synthetically produced from amino acids in a lab seemed dubious. 

However, as it turns out, heme is ubiquitous to many living organisms, and can be found in  bacteria, fungi, protozoa, higher plants, and animals. In fact, the heme used by Impossible Foods Inc. is derived from a plant heme known as leghemoglobin, that is sourced from soybeans. The leghemoglobin is not directly extracted from the soybean, as extracting leghemoglobin from plant roots is tedious and not cost effective due to low yield. Therefore, to increase productivity, the leghemoglobin is synthesized through genetic engineering. Continue reading →

Cold-sore sufferers may be at risk for Alzheimer’s Disease

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

Alzheimer’s disease (AD), the most common cause of dementia, is a neuro-degenerative disease that causes cognitive decline affecting memory and executive function. While rarely due to genetic mutation, the cause of most cases of Alzheimer’s disease is not known. However, new research indicates that the virus that causes cold-sores (fever-blisters) may also cause or contribute to the development of Alzheimer’s disease. Continue reading →