HEALTH

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

Psychologically Transmitted Disease: Heroin Addiction

~ Dr. Stacia Nicholson, PhD ~ 1 Comment

Heroin has regained the attention of the media, as its use is now reported to be of epidemic proportions. According to the CDC (Centers for Disease Control and Prevention) the amount of deaths related to opioids including heroin has quadrupled since 1999 to 2014. Today the incidence of heroin abuse is seen primarily in White males, in young people —both male and female, ages 18-25, and in states occupying the Midwest region of the  United States. The reason for this recent epidemic has been associated with the use of prescription opioid painkillers. In fact, non-medical use of prescription opioids is a major risk factor for heroin use.  In addition, the cost of heroin has decreased,  its purity increased, and its availability is still readily attainable.

With so many people currently dying from heroin, government officials and policy makers are struggling with how to cope with an epidemic that is neither air-borne, vector-borne, or food-borne, but born out of the psychology of pain. Recently, media attention and public debate has surrounded the establishment of heroin clinics as a solution to the death crisis. Addicts may go to heroin clinics to receive injections of heroin, and in case of overdose, the antidote Naloxone (Narcan). Astonishing as it may seem, this is not the first time there has been a heroin epidemic, and neither is the idea of giving heroin to addicts at heroin clinics novel. Continue reading →

A Chemical By Any Other Name : How Cinnamon Can Be Toxic (Part 1).

~ Dr. Stacia Nicholson, PhD ~ 4 Comments

People often think that because something is derived from nature that intrinsically it is safe. However, a chemical is still a chemical regardless of whether it comes from a plant or synthesized in a laboratory. Case in point is Cinnamon and a component of its oil.

I have been suffering for 2 years from re-occurring, sporadic eruptions of a rash all over my face. The skin on my face would first become very itchy and oily, then it would get hot and red. Lastly, it would break-out into what looked like a heat rash, that would prickle, sting, and sometimes burn. Once the flare-up reached its climax, it would subside anywhere from within an hour to a day. Afterwards, it was such that no one would ever know anything was ever wrong with my face. So, when I would go to the dermatologist, they would look at me as if though I was delusional, and tell me it was nothing— perhaps it was just acne.

Yet still, I was prescribed an array of treatments that didn’t work: oral antibiotics, topical antibiotics, topical anti-fungal, oral anti-fungal, hydrocortisone ointment, a sulfur-containing face-wash. Only one doctor confirmed what I had suspected all along; that it was contact dermatitis! The problem was, I still didn’t know what was causing it. I had previously seen an Allergist, I knew for certain I had a serious allergy to dust-mites, oral allergies to a series of fruit whose proteins cross react with my true allergy to birch trees, but nothing prepared me for this:

It was only after careful consideration of my diet and examination of the ingredient list of all the products I had been apply to my skin and hair, that I came to the realization of the culprit. Turns out there is a chemical that is found in Cinnamon known as Cinnamaldehyde. It is used in cosmetics and foods to impart fragrance or flavor. It is a known skin irritant and a strong sensitizer.

Cinnamon or Cinnamaldehyde was in the cinnamon raisin bread and bagels my sister kept in the house, that I would only eat periodically. It was in the cereal my mom would sometimes bring home. I was putting it in the banana bread I started baking. It was everywhere; I was unwittingly exposing myself randomly and repeatedly to Cinnamaladehyde. Primarily, it was in one of the conditioners I  washed my hair with (I wash my hair everyday with conditioner, and sometimes I would rotate brands). This was why it was primarily affecting my face, but re-occurring sporadically. I wasn’t always using a product that contained the chemical, but when I did the majority of it was coming in contact with the skin on my face. I also had hives and clusters of prickly pimple like bumps appearing on my forearms.

NOKIA Lumia 900_004242NOKIA Lumia 900_004333

Now I take an oral anti-histamine each day, and try to stay away from eating and applying anything that contains cinnamon extracts. Cinnamaldehyde is derived primarily from cinnamon bark and other plants, but is also synthesized in a lab. To know more about how and why it causes dermatitis click here for Part 2.

A Chemical By Any Other Name: How Cinnamon Can Be Toxic (Part 2).

~ Dr. Stacia Nicholson, PhD ~ 2 Comments

cinnamaldehyde-04

Cinnamaldehyde (cinnamic aldehyde, cinnamal) is a naturally occurring aldehyde in many plants. The clear yellow liquid is extracted mainly from cinnamon bark (cinnamomum cassia, cinnamomum zeylanicum) and has a strong spicy aroma and sweet taste. For this reason it is commonly used as a flavorant and fragrance in foods, cosmetics, and other products. It has also been commonly reported to cause  allergic contact dermatitis, as it is a known skin irritant and strong sensitizer .

Cinnamaldehyde was first isolated from Cinnamon essential oil in 1834. Cinnamon contains approximately 1 to 3.5% essential oil. The oil itself, is approximately 70 – 90% cinnamaldehyde. The oil has been used to impart such fragrances as almond, apricot, butterscotch, hyacinth, and lilac.  It has been recognized in Europe as the most common organic allergen in humans, second  only to Nickel. In fact, do to its potential for allergenicity, the European Union has listed cinnamaldehyde and cinnamic alcohol as fragrance materials that must be labeled on consumer products (essential oils often appear on labels as : “essential oil mix” or ” natural fragrance”). Continue reading →

What’s Eating at the Lake?

~ Dr. Stacia Nicholson, PhD ~ 1 Comment

A twenty-one year old woman dies in California from “brain-eating” amoeba. A Minnesota teen boy is reported to have died also. Now the same “bugs” have been found in St. Bernard Parish water system in Louisiana. Is this an epidemic? They say it’s rare; if so then why is it so concerning, that its being screened for in some city water systems?

Should I be afraid?

It’s not an epidemic and it is rare, but the problem is it is deadly! The “bug” is small and can’t be seen by the naked eye and most don’t even know of its existence or danger. Also, it is not readily diagnosed because, the symptoms take a long time to show, and they mimic those of bacterial meningitis. By the time doctors even realize what they are dealing with, in most cases, it’s already too late.

life-cycle_web Continue reading →

“On the Spot”: Interview with Veterinarian Nastassia Germain

~ Dr. Stacia Nicholson, PhD ~ 2 Comments

 I have the pleasure of introducing you all to a friend of mine. She has graciously agreed to do an interview for us, in order to help give a better understanding to the public of the real lives of persons in the science and medical field.  Also to give clarity to what these careers actually entail, and most importantly to give a face to the profession.

What is your name, title/current position and where do you work?

My name is Dr. Nastassia Germain, DVM. I currently work at a small animal general practice in Brooklyn and I also do per diem Emergency shifts at a 24 hour emergency hospital. I am actually currently looking to transition from general practice to ER full time. Continue reading →

Water to Wine : Arsenic contamination

~ Dr. Stacia Nicholson, PhD ~ 2 Comments

Toxic wine lawsuit

In recent news, 24 California wineries are being sued for selling arsenic laden wines. According to the news reports, 3 independent laboratories were asked to test over a thousand wines, of which over 80 were shown to contain elevated levels of arsenic. In some cases arsenic concentrations were as high as five times the maximum allowed concentration permissible in drinking water. Drinking water is being used as the standard because the United States does not have any legislation regulating the arsenic content of wine. You might be wondering, why wine producers would knowingly sell wine containing arsenic, whether they put the arsenic in the wine, and how this might affect your future wine consumption endeavors. Before you throw your bottles (or boxes for the matter) of wine down the drain lets explore this situation further.

What is  Arsenic?

Arsenic is a metalloid naturally found in the earths crust. Inorganic and organic forms are released from the environment by anthropogenic use – by peoarsenicple during production of metal alloys, microelectronics, and agriculture. Historically it has been used in fertilizers, in pesticides, in medicines, and in the preservation of wood (like pentachlorophenol ). Worldwide Arsenic exposure is a major environmental and occupational public health issue.

How Arsenic Gets into Wine.

In actuality Arsenic is usually present in wine. This is a direct result of the use of arsenic containing pesticides for grape production. As a result of this use arsenic is present in  soil and  water; contaminating fruits and ground water. The World Health Organization established as a guideline, the maximum concentration of arsenic in drinking water; 10 micrograms per liter.  The major component of arsenic is wine in the inorganic form, which happens to be more toxic than the organic form, however the arsenic content of wine is generally low ( < 10 ppb). Interestingly enough arsenic is also present in beer.

Wine made from grapes that have ripened on the vine longer have a higher amount of arsenic. This makes sense because they have been allowed to take up more arsenic from the soil and water they are grown in. In  addition, the acidity of soil or of wine itself keeps arsenic stable.  Prolonged fermentation during the production of wine could however decrease the presence of arsenic in the final product due to volatilization and sedimentation. Essentially, the fermentation process allows for arsenic to be transformed into other arsenic species that may be less harmful, and easier to remove.

Arsenic toxicity

arsenic2

The amount of arsenic present in wine is  not enough to be immediately toxic. In other words it won’t result in death, however it will result in the excess intake of the element in wine drinkers. The most common routes of exposure to arsenic are oral (drinking water and food ) and inhalation (arsine gas).

The U.S. EPA (environmental protection agency) classifies arsenic as the number one carcinogen. Chronic exposure is known to cause cancers of the skin, lung, bladder, kidney, and liver. It also predisposed humans to the development of cardiovascular disease, diabetes, pulmonary diseases, and neurological impairment. Hallmarks of chronic arsenic toxicity are skin lesions; hyperpigmentation and keratosis.

Arsenic can be detected in the urine, and is a good indicator of exposure within 1-2 days of ingestion. Fingernails and hair can be used to detect acute (sudden large doses) exposure to arsenic up to 6 to 12 months after exposure.  The only treatment for acute arsenic toxicity is to treat the symptoms. Chelation therapy is limited in its ability as it may reduce the amount of arsenic in the body, but it won’t undo the harm that is already done.

Summary

California wine producers have rebutted that the lawsuit is egregious and might result in an unnecessary loss of confidence by consumers in wineries. In all honesty, only approximately 6 percent of the wines tested were shown to contain high levels of arsenic. Although the U.S. does not have any laws regulating arsenic levels in wine, the European union does. Wine producers assert that they maintain these guidelines as standards in their production. Also, the wines that are most culpable are cheap wines; like box wines. Buying quality expensive wine will reduce your risk of being exposed to high levels of arsenic, this is likely true, due to longer fermentation (aging), and better processing; such as filtration and removal of pulp. It might be wise for there to be government regulation and monitoring of arsenic levels in wines produced and sold in the United States. The issue of arsenic being present in wine is not unique to American wines, it also occurs in European wines and to a lesser extent; beer. It may be impossible to remove all arsenic from wine and even water for that matter, what is important is that it not be present in quantities that exceed those to which pose no significant harm to human health.

“PENTA”…More than greek for the number 5.

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

I was watching the news a little over a week ago when I heard them talking about something called “penta” that was being applied to telephone/electric poles and that senator Chuck Schumer was upset about it possibly getting into the groundwater. For the life of me, I had no idea was they were talking about, but I did know that “penta” could not be the proper name for the chemical in question. I tried googling “penta + chemical” and I got nothing meaningful in the way of results. So, I went to my mentor and said “what is this chemical they are painting onto wood poles that has everyone so upset? I can’t remember the name they called it on the news, but it sounds incomplete.” He said oh yes, a wood preservative, they have been using it for years”.

So what is “Penta”

Penta is a synonym for the chemical Pentachlorophenol that is currently used as a wood preservative. It is an organochlorine pesticide, okay, why didn’t they just say so? I know all about organochlorines and their toxicity! I’m guessing, they didn’t really know much about what they were covering, they just knew it was important, and sounded bad.

Is Pentachlorophenol (PCP) bad?

Since the 1980’s the use of PCP has been restricted in the United States, and it’s use and manufacture is banned in several countries, such as Germany, throughout the world. In the U.S. it is only manufactured by one company – Vulcan chemicals. The problem is that it is a major, ubiquitous (found everywhere), environmental contaminate. It’s presence in groundwater and soil causes the most concern, because it can get into foods such as fruits, vegetables, and grain, as well as into drinking water. This is mostly due to its previous widespread use in agriculture and as a pesticide, where it was also available for  commercial use in and around homes and gardens. It was first registered as a wood preservative in the U.S. during the 1930’s. It has also been registered for use as an insecticide, herbicide, algicide, fungicide, germicide, and molluscicide . Pretty much it’s a biocide, meaning it kills a lot of different living things. Common exposure to the chemical by humans won’t result directly in death, but it can cause substantial harm. It is toxic to both animals and humans in acute and long-term exposures. Meaning, that if you are exposed to large amounts at one time, or if you are exposed to low amounts over a long period of time, it could have serious negative affects on your health.

What are the side affects of PCP and how are you exposed?

The type of exposure describes above can result in liver, kidney, blood, lung, nervous system, immune system, and gastrointestinal disease. This is due to the chemicals ability to disturb energy metabolism in the body (the way ATP is used) that leads to energy being  redirected into heat production.  As a result, acute signs and symptoms of exposure to PCP are tachycardia (fast heart beat), increased respiratory rate, fever, metabolic acidosis, and perfuse sweating. More serious complications are: aplastic anemia, leukemia, Hodgekins disease, and non-Hodgekins lymphoma. You can be exposed to PCP through 3 routes: oral, dermal, and inhalation. You can breathe in the vapors that are evaporating from wood poles or you can inhale its dust particles. You can also absorb it through your skin if you come in contact with it by touching or leaning onto a surface treated with PCP. Orally, you can be exposed to PCP by ingesting it from food or drinking water; children  by eating soil. If you live in a house (mostly log cabins) that has wood treated with PCP you are at higher risk of exposure through inhaling its vapors or breathing it dust particles from wood splintering and chipping away.  If you live near a hazardous waste site that disposes of PCP, or factory that manufactures it you are also at higher risk of exposure. Burning PCP treated logs can cause eye and respiratory tract inflammation because it produces an irritating and toxic gas.

In Summary

Pentachlorphenol is a synthetic chlorophenol chemical containing 5 chlorine molecules, along with carbon, oxygen, and hydrogen.  Listed as a probable human carcinogen, its use is regulated and only permissible to certified applicators. It is predominately used for the treatment of wood and in railroad ties, cross arms, and fence posts. It is no longer available for use by the general public or as a pesticide, thereby its prevalence in the environment has since declined significantly. It is degraded by sunlight in the air and surface water, and by microbes and organisms in soil. However effluents from factories and waste sites still present a source by which PCP can enter the environment. The most significant risk exposure is occupational, meaning that workers who apply or manufacture PCP are most at likely to suffer harm. You can reduce your exposure by washing and peeling fruits and vegetables. The Food and Drug Administration monitors PCP levels in food and it is not shown to buildup in the food chain. It is eliminated from your body via urine, but can be measured in your blood and found in your body fat.

What Ever Happend to Ebola?!

~ Dr. Stacia Nicholson, PhD ~ Leave a comment

In March of 2014 the World Health Organization (WHO) announced the outbreak of Ebola in Guinea. Subsequently, the disease spread to Guinea’s bordering countries; primarily Sierra Leone and Liberia.  Then it spread to Nigeria and Senegal, and a few cases were imported to Spain and the U.S. by way of missionary work in certain parts of Africa. It was during this spread outside of Africa that mass media coverage became frenzied and Americans flew into a panic. People were calling for closed borders, African immigrants were being ridiculed, heated racial debates surrounding Zmapp arose, and people on a whole were afraid of it hitting their city. Then all of a sudden there was quiet, so what happened to Ebola? Well, nothing happened to it, it’s still there as it’s been for about 4 decades since its first reported outbreak in 1976. Ebola has actually broken out 16 times since, the difference now is that this outbreak is the largest outbreak of Ebola ever. Contrary to popular belief  it is actually the first outbreak of Ebola in West Africa! Never before had it broken out in such populated regions; allowing for it to be more easily spread.

What is Ebola?

Ebola is a virus in the family of Filoviridae along with Marbug virus, that causes Hemorrhagic Fever. The virus leads to hemorrhaging by causing the body to lose the ability for your blood to clot, through multiorgan damage and drop in blood pressure. There are actually several Ebola viruses: Sudan Ebola, Zaire Ebola, Cote D’Ivoire Ebola, and Bundibugyo Ebola.  They are all distinct species of Ebolavirus. The virus got its name from a small river in northwestern Democratic Republic of the Congo (DRC).

History

In 1976 the first cases of  Ebola were documented in Sudan and DRC (formerly Zaire), regions of Central Africa;  where it is endemic.  Then came Cote D’Ivoire Ebola in 1994; a third species. The latest type of Ebola to emerge was Bundibugyo Ebola in 2007. All of these species of Ebola are known to cause Hemorrhagic fever in humans and non-human primates. There is another Ebola virus called Reston Ebola virus that unlike the others is  not known to infect humans, and originates outside of Africa. Found in the Philippines, Reston Ebola infects monkeys and pigs.  The recent 2014 outbreak was caused by Zaire Ebola, one of the most deadly forms.

outbreak-distribution-map
http://www.CDC.gov

Myths and Misunderstanding

Some people mistake Ebola for an airborne disease because of how easily it is transmitted. However, it is can only be contracted through direct contact with an infected person bodily fluid such as blood, saliva, nasal discharge, and even semen.

Since it is spread through bodily fluid, another misconception is that the virus is like HIV; the two viruses are not related in any way. Ebola can kill you in a matter of days to weeks, HIV cannot. HIV is primarily spread through sexual intercourse or must enter your bloodstream (needle-use) in order for you to be infected. Ebola can be transmitted via oral administration, such as eating raw or undercooked meat from bats, which act as a reservoir for the virus.

A major controversy arose after the investigational vaccine ZMAPP was administered to Kent Brantly, MD. Many people feared that the government or pharmaceutical companies were withholding a cure from the general public. After a black man seeking treatment fled to the U.S. died from the infection, some people claimed he was denied the vaccine because of his race, and further erroneous claims came forth that the vaccine only works in caucasians. Three Liberian doctors also received the investigational vaccine, one still died. There are no current preventative or curative medicines against Ebola approved for human use.

What now?

The Majority of victims of this latest Ebola outbreak were in West Africa. As of October 2014, according to WHO 8,914 infections had been documented and  of those 4,447 were fatal. Ebola remains a global public health threat due to lack of treatment and it being a “high-mortality” disease. In previous decades, because outbreaks were rare and confined to remote areas there was little interest by companies to undergo the costly development of a vaccine. However, with increasing and recurring resurgences, the possibility of imported infections, and the potential misuse of the virus as a bioterrorist agent, several pharmaceutical companies are in the early stages of developing a treatment for Ebola Hemorrhagic Fever.  The best method of control is to confine the disease when it presents itself , treat the symptoms and supply supportive care to patients, and educate public health officials and agencies on methods to mitigate the spread of the virus. Isolating infected persons, disinfecting the environment, and using personal protective equipment while treating Ebola cases is what’s recommended by the Center for Disease Control. Ebola continues to pose little threat to Americans.

Measles Outbreak

~ Dr. Stacia Nicholson, PhD ~ 2 Comments

By now we’re all familiar with the recent Measles outbreak in California, stemming from Disneyland. We also are familiar with the controversy associated with it’s spread and the anti-vaccination movement. What we all might not be familiar with are the facts and history of Measles, and why it’s so important. Is it all just media hype and fear mongering, to make the pharmaceutical companies rich, or is there real danger and a reason for concern?

What is Measles?

Measles is not a bacteria, it is a virus, you cannot treat it with antibiotics. Measles is one of the leading childhood diseases worldwide, but adults can contract it too. Only humans are known to get Measles,  it is not spread from some wild animal somewhere. You can only get it from another human being. With that being said, it is an infectious disease, meaning it is highly contagious. If you are exposed to it without having immunity, there is a 90% assurance that you will develop the disease.

How is it spread?

The Measles virus is spread through the air via droplets from  someone coughing or sneezing, making crowded and enclosed places like stadiums, airplanes, dorms, schools, and urban cities prime location for its transmission. It infects your lungs first before moving to your lymphatic system, where it then spreads throughout the rest of your body. Once you’ve been infection anywhere from 8 to 12 days can pass before you begin to show symptoms. This is one reason why it is so communicable. People who do not know they are infected can spread it to their families, coworkers, and anyone else they come in contact with without even knowing it. You become contagious 1 day before symptoms appear and up to 4 days after the rash subsides.

What are the signs and symptoms?

Infected persons will experience a runny nose, irritability, red eyes, cough and fever. The disease is characterized by small grayish white spots in the mouth and throat, and a blotchy red rash that spreads from the face down until it covers the body. The virus suppresses your immune system. As a result, a secondary bacterial infection could develop, this can be treated with antibiotics, but measles itself has no cure. Only the symptoms can be managed; drugs to lower fevers, and fluids to maintain hydration. Once you’ve had measles, you cannot get it again, if you survive you will acquire life long immunity. There are however some complications that could arise from the Measles such as, pneumonia and encephalitis, which can be fatal.

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Measles Outbreaks

My generation grew up with chickenpox, similarly previous generations routinely got childhood diseases like measles, mumps, rubella, polio, and scarlet fever. Polio has been eradicated, and now there is a vaccine against chickenpox. With the advent of the first Measles vaccine in 1963 and the subsequent MMR(measles, mumps, and rubella) vaccine in 1972, a mass campaign was set out to immunize all school age children. Measles was on its way to being eradicated in the Western hemisphere, until 1998 when Dr. Andrew Wakefield published an article in the Lancet claiming an association between vaccines and, autism and bowel disease. It was later withdrawn from the journal, found to be erroneous, and further disproven by the science community. However, the media did not spread the good news, parents became fearful, and the anti-vaccination movement was birthed.

There have been several Measles outbreaks before. From 1989 to 1991 more than 55,ooo cases were reported with 130 resulting in death. Then again from 1993-1995 there was about 300 more cases reported in the U.S. in which victims were unvaccinated. In 2005 and 2006 there were outbreaks in Indiana, and Boston respectively. Current strains  stem from Europe an Asia, where the disease still occurs. In 2013, there was an increase in Measles outbreaks in England, France, and Spain. So, travelers from other countries that do not immunize can bring in the disease, and traveling un-vaccinated can also expose you to the Measles while abroad.

Even if you are vaccinated, you can still get Measles. Yes, you read correctly, you can still get Measles if you have been vaccinated, however if you do it will be much milder. The reason for this, is as you age the immunity you gained from your childhood vaccination may wane, or decrease. The amount that this happens differs from person to person, and can only be assessed by your doctors. This is the reason you have heard medical officials suggest a booster shot for adults as a result of the recent outbreak. It is not a scheme for “big pharma” to make more money. Another reason is that some people who have been vaccinated never acquired immunity, this doesn’t happen often, and to prevent this from occurring a 2 dose vaccine has been employed. The first is given as early 1 year of age to the start of pre-k/kindergarten. The second dose can be given any time after. However, of those recently infected, most were of the population that has not been vaccinated. Those who have been vaccinated will have protection for at least 27 years. Some people are not vaccinated for good reason. These include, cancer patients, those with HIV/AIDS, and other immunosuppressive illnesses, pregnant women, and babies under 1 year of age. Newborns acquire immunity from their mothers, this immunity however is only short-lived.

Thus far, measles outbreaks have occurred recently in the U.S., Canada, and Mexico. It was once near complete eradication in the western hemisphere and other developed countries, it’s still a major problem in Africa and the East. There are efforts worldwide to eliminate this disease completely. As long as human hosts exist whom are capable of carry and spreading the disease there will be outbreaks. This is why vaccine compliance is required. As vaccinations go down, those with natural immunity die off (people who had it and survived), and the immunity of an aging population wanes, heard immunity goes down. With heard immunity lowered, the virus has the chance to spread and infect those who are susceptible and unvaccinated.  The good news is that once an outbreak has passed through a community, all those who have been exposed will become immune for life, and those who have been vaccinated will have their immunity boosted naturally.