Vitamin C And Aging – Aging? Well, it’s not me, I’m still young. But the fact is aging can come to everyone at any time because aging does not always depend on how old you are, but there are several conditions that can cause premature aging.

This time, we want to talk about skin aging. Most people don’t recognize the signs of aging until their 30s or 40s and some people never bother with aging their skin before someone says “ah, why do you look older this time? You are younger than me”. When you know you are 29 but everyone tells you that your face looks older than your age, than the time when you started taking care of your skin and changing your daily routine for your skin.


What is Skin Aging?

Kirkwood and Austad (2000) said, aging is usually defined as a progressive loss of function accompanied by decreased fertility and increased mortality advancing age. So, the theory says it is a loss of function and progressive aging can affect all systems in our body. But, what about aging skin? Should I worry about skin aging? I’m only in my 30’s.
Even though we are young, research says that we can also experience skin aging. This Study says “premature skin aging”. What is that???? Premature? So skin aging will come to you like no one would predict right?

Premature skin aging caused by long-term exposure to ultraviolet irradiation from sunlight. Long-term sun exposure contains more UVB ultraviolet and UVA. UVA irradiation activates ROS (are free radicals, an unstable type of molecule that contains oxygen and which readily reacts with other molecules in cells. Constructed from oxygen species reactions in cells can cause damage to DNA, RNA, and proteins and can lead to cell death) signals from activating the ROS system cause DNA damage.

Skin Aging and Its Characteristics

Skin aging is a complex biological process consisting of two components, intrinsic aging and extrinsic aging. Intrinsic aging is also called true aging which is an inevitable change that is caused by the passage of time alone and is manifested mainly by physiological changes with subtle consequences but undoubtedly essential for healthy and healthy skin and is largely genetically determined. Extrinsic aging is caused by environmental exposure, especially to UV rays, and the more commonly called shooting. The intrinsic rate of skin aging in any individual can be affected dramatically by personal and environmental factors, particularly the amount of exposure to ultraviolet rays.

Photodamage, which significantly speeds up visible aging of the skin, also greatly increases the risk of skin cancer. Intrinsic aging is an inevitable physiological process that results in thin, dry skin, fine wrinkles and gradual dermal atrophy, while extrinsic aging is provided by external environmental factors such as air pollution, smoking, poor nutrition, loss of elasticity, and the appearance of aging skin.

Vitamin C and Aging Skin

Vitamin C (ascorbic acid) is the most abundant antioxidant in human skin, forming part of a group of enzymatic and non-enzymatic antioxidant complexes that coexist to protect the skin from reactive oxygen species (ROS). Vitamin C is water-soluble, functions in the chest compartment of cells. When the skin is exposed to UV rays, ROS such as superoxide ions, peroxide and singlet oxygen are generated. Vitamin C protects the skin from oxidative stress by sequentially donating electrons to neutralize free radicals. The oxidized forms of vitamin C are relatively non-reactive. Furthermore, they can be converted back to Vitamin C by the enzyme dehydro acid acid reductase in the presence of glutathione. Exposure to UV rays can reduce the availability of Vitamin C in the skin.

Antioxidants are required to neutralize the ROS formed due to UV exposure. It is important to note that Vit C is equally effective against UVB (290-320 nm) and UVA (320-400 nm) . Repeated small doses of UVA penetrate 30-40 times deeper into the dermis as it fights UVB, which mostly affects the epidermis. UVA mutates and destroys collagen, skin elastin, proteoglycans (proteoglycans support hydration of normal skin extracellular matrix, providing resilience, viscoelasticity, and a soft environment conducive to cellular function and development ) and other skin cellular structures. Thus, UVA causes UVB skin to cause sunburn, ROS, epidermal mutations (mutations that occur in the outer layer of the skin) and skin cancer. Sunscreen when applied properly prevents UV-induced erythema (is a type of skin rash caused by injured or inflamed blood capillaries) and other serious skin problems. However, sunscreen only blocks 55% of the free radicals generated by UV exposure. Photoageing (premature aging) can be prevented by preventing UV-induced erythmias, sunburn cell formation and inducing collagen repair. To optimize UV ​​protection, it is important to use sunscreens in combination with topical antioxidants. Vit.C does not absorb UV rays but provides a UV protective effect by neutralizing free radicals, while this effect is not seen with sunscreens. Under laboratory conditions, it has been shown that application of topical Vit 10% .C showed a statistical reduction of UVB-induced erythema by 52% and sunburn cell formation by 40-60% .

Vitamin C also directly activates the transcription of collagen synthesis and stabilizes procollagen mRNA, thereby regulating collagen synthesis. Clinical studies have shown that topical use of Vit.C increases collagen production in young as well as aging human skin. Some studies also suggest Vitamin C as a depigmenting agent, but vitamin C is often combined with other depigmenting agents such as soy and liquor for better depigmenting effects. Vitamin C interacts with copper ions at the tyrosinase-active site and inhibits the action of the tyrosinase enzyme, thereby reducing melanin formation.

How Can You Find Vitamin C ?

Vitamin C is found in citrus fruits, such as oranges, lemons and grapefruit, amla, tomatoes, sprouted grains and green leafy vegetables. For lemons, lemons contain 77mg of vitamin C per 100 grams, with one medium lemon providing 92% of the DV. For adults, the recommended daily amount of vitamin C is 65 to 90 milligrams (mg) daily and the upper limit is 2,000 mg daily. Be careful, too much dietary vitamin C is unlikely to be harmful, taking vitamin C supplements can cause diarrhea, nausea, vomiting, heartburn, stomach cramps, headaches and insomnia.13 You can also get vitamin C injections into your veins. But keep in mind, however, that you have to go to your doctor to do this.


  1. Thomas B. L. Kirkwood, Steven N. Austad. Why do we age. NATURE. 2000. VOL 408. DOI: 10.1038/35041682 · Source: PubMed
  2. Uraiwan Panich, Gunya Sittihumcharee, Natwarath Rathviboon, Siwanon Jirawatnotai. Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging. Hindawi Publishing Corporation Stem Cells International Volume 2016, Article ID 7370642, 14 pages
  3. Assaf H., Adly M.A., Hussein M.R. (2010) Aging and Intrinsic Aging: Pathogenesis and Manifestations. In: Farage M.A., Miller K.W., Maibach H.I. (eds) Textbook of Aging Skin. Springer, Berlin, Heidelberg.
  4. Shoubing Zhang, Enkui Duan. Fighting against Skin Aging: The Way from Bench to Bedside. SAGE. Cell Transplantation 2018, Vol. 27(5) 729–738 ª The Author(s) 2018 Reprints and permission: DOI: 10.1177/0963689717725755
  5. Wikipedia. Vitamin C. Access : March 6 2021
  6. Pumori Saokar Telang. Vitamin C in Dermatology. Indian Dermatol Online J. 2013 Apr-Jun; 4(2): 143–146. doi: 10.4103/2229-5178.110593
  7. Traikovich SS. Use of Topical Ascorbic acid and its effects on Photo damaged skin topography. Arch Otorhinol Head Neck Surg. 1999;125:1091–8
  8. Matsuda S, Shibayama H, Hisama M, Ohtsuki M, Iwaki M. Inhibitory effects of novel ascorbic derivative VCP-IS-2Na on melanogenesis. Chem Pharm Bull. 2008;56:292–7.
  9. Margaret Mary Smith, James Melrose. Proteoglycans in Normal and Healing Skin. Adv Wound Care (New Rochelle). 2015 Mar 1; 4(3): 152–173. doi: 10.1089/wound.2013.0464
  10. Farris PK. Cosmetical Vitamins: Vitamin C. In: Draelos ZD, Dover JS, Alam M, editors. Cosmeceuticals. Procedures in Cosmetic Dermatology. 2nd ed. New York: Saunders Elsevier; 2009. pp. 51–6.
  11. Burke KE. Interaction of Vit C and E as better Cosmeseuticals. Dermatol Ther. 2007;20:314
  12. Draelos ZD. Skin lightening preparations and the hydroquinone controversy. Dermatol Ther. 2007;20:308
  13. Katherine Zeratsky, RD, LD. Is it possible to take too much vitamin C?. Acces :

vitamin c and aging vitamin c and aging vitamin c and aging



Sunrays Makes Skin Problems – I remember back when I was a little. My skin is so soft, no worries with sunburn, acnes problem, dry skin etc. But later on, I knew that I must be more concerned about how sunrays makes skin problems with my skin. When everyone wanted to get tanned, another wanted to get much brighter. Truly I tell you, all those things maybe can impact our skin condition and can cause many problems later.

This time, I want to share with you about how sun rays can effectively cause skin damage in short or long period of time. Sunrays makes skin problems that can cause sunburn, also aging! Ladies, ageing makes us more worries than before. Skin ageing and dehydration causes by several things. The environment, the UV light, from the medication that you take, any medical conditions (ex: cancer, hypothyroidism ).


Figure 1. Skin Anatomy (source: WebMd © 2014 WebMD, LLC. All rights reserved. )

Skin represents our barrier against the environment and it consists in 3 layers: Hypodermis (deepest layer) which consisted by adipose tissue, vessels, and nerves. Dermis (middle layer) consisted by connective tissue, there are collagen and elastin fibers, blood vessels, oil glands, hair follicles, sweat glands. The third is Epidermis (the outer layer) consisted by keratinocytes. Keratinocytes are the primary type of cell in the epidermis, the outermost layer of the skin. IN humans, they constitute 90% of epidermal skin cells.1 Keratinocytes, localized in the stratum corneum (stratum corneum is the outermost layer of keratinocytes which continuously shed and replaced). Stratum corneum provides skin hydration and in particular, lipids play a significant role against evaporation holding water. Sweat and oil glands products, skin natural moisturizing factors, participate to moisture content maintenance, acting as endogenous humectants.2


Our skin normally get exposed to the sun exclusively to wavelengths <294 nm, while solar ultraviolet radiation, which contains both UVA (320-499 nm) and UVB (290-320 nm), might cause injuries to the skin. UVA penetrates deeper than UVB into the skin layer and mediates damage to both the epidermis and dermis.3 Numerous reports have shown that UV radiation, including UVA and UVB, significantly disturbs the human skin cells production which skin will overproduction of reactive oxygen species/ROS (are free radicals, type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A build up of a reaction oxygen species in cells may cause damage to DNA, RNA, and proteins and may cause cell death), which impair antioxidant system such as thioredoxin and glutathione-glutathione peroxidase. Glutathione peroxidase is an intracellular antioxidant enzyme to protect skin from harmful effects of the external exposure. Thioredoxins are proteins in human body that act as antioxidants by facilitating the reduction of other proteins by biosynthesia in cell and help to controls expression of numerous inflammatory genes. In addition, thioredoxin has general intracellular antioxidant activity and when upregulated or overexpressed, protects against oxidative stress4 (is a phenomenon caused by an imbalance between production and accumulation of oxygen reactive species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products).

Even sunrays makes skin problems, but human still needs the benefit of the sun rays, we still need to know which time is best sun light to our health. Because some studies says that suns’s rays may shrink fat cells below our skin, so it’s very important to know which the perfect time. Morning light estimated at 8 am and noon above 4pm it’s the safest time, which the ultraviolet concentration wasn’t high as 10 am to 4 pm. Vitamin D can actively be produced by the time we exposed to sunlight, sun exposure is by far the best way to boost our vitamin D levels.

But, what happen if we get overexposure from sunlight? What skin problem that we get?

Sun exposure can cause skin aging, and right sun’s ultraviolet light damages the fibers in the skin called elastin. When these fibers break down, the skin begins to sag, stretch, and lose its ability to go back into place after stretching5. UV also causes the immunologically important epidermal Langerhan’s cells(cells location at the skin barrier and role as immune sentinels) to be inactivated and lost. Further effects of UV exposure include thickening of the epidermis and an increased production of melanin, a pigment produced by melanocytes that is responsible for tanning of the skin and some natural protection against future exposure. Environmental damage to the skin is associated with several neoplastic conditions commonly seen in the elderly, including actinic keratosis , Bowen’s disease , squamous cell carcinoma , and basal cell carcinoma.6 Risk of skin cancer is heavily influenced by UV exposure and by skin pigmentation.

Figure 2. Influence of pigmentation on skin cancer risk. Fair-skinned individuals with low levels of melanin(skin pigment) in the epidermis display a UV sensitive phenotype, tending to burn rather than tan, after UV exposure. Recent data suggest that mutations that contribute to fair complexion and tanning impairment, specifically signaling defects in the melanocortin 1 receptor/MC1R (is a protein that works like receptor in our skin, that regulates skin pigmentation, UV responses, and melanoma risk) may also be associated with less efficient DNA repair in melanocytes(cells that produces melanin/pigment). MC1R-defective individuals not only suffer higher realized doses of UV radiation because their skin is less able to block UV photons, but they may also accumulate more mutations from UV exposure because of defective DNA repair.

One of the most obvious acute effects of UV include erythema (sunburn), pigmentation (tanning), suppression of acquired immunity, and enhancement of innate immunity, all mostly caused by UVB.8 UVB induces a cascade of cytokines, vasoactive and neuroactive mediators in the skin that together result in an inflammatory response and causes “sunburn”.7


We are all familiar with sunscreen, right? So, its not just myth that our skin really needed protection to get blocked ultra violet from sun rays that can harmful to our skin and causes skin problems. Sunscreens were originally developed to minimize sunburn, but the action spectrum which shows more effective in UVB then UVA. Sun protection factor as we know as SPF mainly specific to protect against the UVB. And all we think that the higher SPF is, the higher protection we got from against UVA and UV, but that’s not true. SPF 30 blocks 97% of UVB rays and SPF 50 blocks 98% of UVB rays.9

Since SPF only applies to UVB rays, it’s imperative to choose a sunscreen that says “broad spectrum” on the label, as this indicates the product helps protect the skin from UVA rays as well.9 The Skin Cancer Foundation recommends applying sunscreen 30 minutes before going outside, then reapplying every two hours and immediately after swimming or sweating. No sunscreen is waterproof, only water-resistant.9 We must also have to considered about the skin cancer, because sunscreen alone is not enough. We still have to do extra protection such as shade and covering our skin with cloth, wide-brimmed hats and UV-blocking sunglasses.


  1. Wikipedia. Keratinocytes. Access 2 March 2021
  2. American Skin Association. Dry Skin. , Access 2 March 2021
  3. Pei-Wen Wang, Yu-Chiang Hung, Tung-Yi Lin, Jia-You Fang, Pei-Ming Yang, Mu-Hong Chen, Tai-Long Pan. Comparison of the Biological Impact of UVA and UVB upon the Skin with Functional Proteomics and Immunohistochemistry. MDPI. Antioxidants (Basel). 2019 Dec; 8(12): 569. Published online 2019 Nov 20. doi: 10.3390/antiox8120569.
  4. Elias S. J. Arner, Arne Holmgren. Physiological Functions of Thioredoxin and Thioredoxin Reductase. European Journal of Biochemistry. First published: 25 December 2001. . Access: March 3 2021.
  5. Cosmetic Procedure: Sun Exposure and Skin Cancer. .Access: March 4 2021
  6. Chronic and Acute Effects of Sun Exposure on the Skin. Mary Ann E. Zagaria, PharmD, MS, CGP
    Senior Care Consultant Pharmacist and
    President of MZ Associates, Inc., Staten Island, New York. US Pharm. 2007;32(4):20-26.)
  7. John D’Orazio, Stuart Jarret, Alexandra Amaro-Ortiz, Timothy Scott. UV Radiation and the Skin. International Journal of Molecular Science. Int J Mol Sci. 2013 Jun; 14(6): 12222–12248. Published online 2013 Jun 7. doi: 10.3390/ijms140612222
  8. Antony R. Young. Acute effects of UVR on Human Eyes and Skin. Prog Biophys Mol Biol 2006 Sep;92(1):80-5. doi: 10.1016/j.pbiomolbio.2006.02.005. Epub 2006 Feb 28
  9. Sunscreen 101: How to Get the Most out of Your Sun Protection Products. access: March 5 2021


Coronavirus Vaccine Comparison – All of vaccines are typically need years for research and testing before it can be used clinically. But some of situation not required that because of emergency state happen in this pandemic era of Corona virus. The emergency of needing the vaccine as one of the prevention step to stop the spreading of the virus so each country developed their own research to make the best vaccine to help their own country and to help our world so we can fight and stand against the COVID-19 together.

So many vaccines are developed in each country around the world. But not all the vaccines are ready to be used. Researchers are currently testing 67 vaccines in clinical trials on humans, and 20 have reached the final stages of testing. At least 89 preclinical vaccines are under active investigation in animals. Some of us maybe didn’t understand about clinical trials, vaccine trials etc. But here some of the information about coronavirus vaccine comparison.1

Also Read COVID-19 and DIABETES

I. The Vaccine Testing Process

An ideal SARS-CoV-2 vaccine, to fight the pandemic, should have the following features:2

  1. Elicit long-lasting protective immune responses;
  2. Should be given to everyone regardless of comorbidity or age, immune status, pregnancy/breastfeeding status;
  3. Lack the potential to cause antibody dependent enhancement (ADE) or pulmonary immunopathology;
  4. Should be thermostable in order to enable transportation and storage in developing countries with poor refrigeration facilities;
  5. Be highly immunogenic in the general population including a population with preexisting anti-vector antibodies.

An experimental vaccine is first tested in animals to evaluate its safety and potential to prevent disease. It is then tested in human clinical trials, in three phases:

  • Phase I – in phase I, the vaccine is given to a small number of volunteers to assess its safety, confirm it generates an immune response, and determine the right dosage.
  • Phase II – in phase II, the vaccine is usually given hundreds of volunteers, who are closely monitored for any side effects, to further assess its ability to generate an immune response. In this phase, data are also collected whenever possible on disease outcomes, but usually not in large enough numbers to have a clear picture of the effect of the vaccine on disease. Participants in this phase have the same characteristics (such as age and sex) as the people for whom the vaccine is intended. In this phase, some volunteers receive the vaccine and others do not, which allows comparison to be made and conclusions drawn about the vaccine.
  • Phase III – in phase III, the vaccine is given to thousands of volunteers – some of whom receive the investigational vaccine, and some of whom do not, just like in phase II trials. Data from both groups is carefully compared to see if the vaccine is safe and effective against the disease it is designed to protect against.

Once the results of clinical trials are available, a series of steps is required, including reviews of efficacy, safety, and manufacturing for regulatory and public health policy approvals, before a vaccine may be introduced into a national immunization program.3

Early or Limited Approval : many countries have given emergency authorization from their government based on preliminary evidence that they are safe and effective.1

Approval : regulators review complete trial results and plans for vaccine’s manufacturing, and decide wheter to give it full approval.1

Combined Phase : one way to accelerate vaccine development is to combine phases. Some vaccines are now in Phase ½ trials, for example, which this tracker would count as both Phase 1 and Phase 2.1

Paused or Abandoned : if investigation observe worrying symptoms in volunteers, they can pause the trial. After an investigation, the trial may resume or be abandoned.1


Table 1. Lead SARS-Cov-2 candidate vaccines with EUA granted, in phase III trials, or licensed (prior to phase III trials)3.

coronavirus vaccine comparison

φ Storage or transportation temperature. * SU not defined in trial. A amount of 3 µg was proposed for a phase III trial [30]. 1x = 1 immunization. 2x = 2 immunizations. VP = virus particles. NA = not applicable. ** Phase I/II studies used two different doses: 5×1010 and 1×1011 virus particles [31]. *** Phase I/II studies used 1×1011 virus particles/dose [32]. # Two versions are available: a frozen version and a lyophilized version, Gam-COVID-Vac-lyo, to be reconstituted. % Approved for use in Chinese military. € Approved for use in Russia. ∑ EUA granted. $ NAAT = nucleic acid amplification test.

coronavirus vaccine comparison
coronavirus vaccine comparison
1.Pfizer(New York) and BIONTECH (German)Comirnaty (also known as tozinameran or BNT162b2
2.Moderna(Boston) and National Institute of HealthmRNA-1237
3.AstraZaneca(Swedish company) and University of Oxford (England)AZD1222 (also known as Covishield in India )
4.Gamaleya Research Institute (Russia)Sputnik V (also known as Gam-Covid-Vac)
5.Sinovac Biotech (China)CoronaVac (formerly PiCoVacc)
6.Johnson & Johnson/JensenAd26.COV2.S
Coronavirus vaccine comparison by name.
  1. Pfizer-BioNTech4

The Pfizer-BioNTech COVID-19 vaccine was sent to the FDA for possible Emergency Use Authorization (EUA) on Friday, November 20 and authorized on December 11. It is an mRNA vaccine that codes for the virus’s spike protein and is encapsulated in a lipid nanoparticle. Once injected, the cells churn out the spike protein, triggering the body’s immune system to recognize the virus. In Phase III trials, it demonstrated 95% efficacy. The Pfizer-BioNTech vaccine requires storage at about -94 degrees F, which requires specialized freezers.

Type: mRNA

Doses: 2, 21 Days Apart

EUA Date: December 11, 2020

Price: $19.50 per dose for first 100 million doses

Efficacy: About 95%

Status: Approved in Several Countries-Emergency use in U.S, and elsewhere

2. Moderna

On November 16, Moderna issued a preliminary data readout out of its COVID-19 vaccine, suggesting an efficacy rate of 94.5%. It was authorized by the FDA on December 19. Like the Pfizer-BioNTech vaccine, it is an mRNA vaccine. Unlike that vaccine, however, the Moderna vaccine is stable at 36 to 46 degrees F, about the temperature of a standard home or medical refrigerator, for up to 30 days and can be stored for up to six months at -4 degrees F. It is expected to go to the FDA for consideration for an EUA within days.

Type: mRNA

Doses: 2, 28 Days Apart

EUA Date: December 18, 2020

Price: $25-$37 per dose

Efficacy: About 95%

Status: Approved in Switzerland, Emergency use in U.S., E.U., Elsewhere

3. AstraZeneca-University of Oxford

On November 23, AstraZeneca and the University of Oxford announced high-level results from an interim analysis of their COVID-19 vaccine, AZD1222. The analysis was from the trials in the UK and Brazil and demonstrated efficacy of up to 90%. The vaccine was effective at preventing COVID-19, with no hospitalizations or severe cases in people receiving it. There were a total of 131 COVID-19 positive cases in the interim analysis group. One dosing regimen was given at a half dose and demonstrated 90% efficacy, followed by a full dose at least one month apart. Another dosing regimen demonstrated 62% efficacy when given two full doses at least one month apart. The combined analysis showed average efficacy of 70%. The AstraZeneca vaccine can be stored, transported and handled at normal refrigerated conditions, about 36-46 degrees F for at least six months and administered within existing healthcare settings.

The AstraZeneca and University of Oxford’s vaccine uses technology from an Oxford spinout company, Vaccitech. It deploys a replication-deficient chimpanzee viral vector based on a weakened version of a common cold virus (adenovirus) that causes infections in chimpanzees. It contains the genetic materials of the spike protein. After vaccination, the cells produce the spike protein, stimulating the immune system to attack the SARS-CoV-2 virus.

Type: Adenovirus-based

Doses: 2, 28 Days Apart

Likely EUA Date: Authorized in Europe on January 12, 2021, and other countries, but unlikely in the U.S. until spring

Price: $25-$37 per dose

Efficacy: Currently about 70% overall

Status : Emergency use in Britain, E.U., Elsewhere 

4. Russia’s Sputnik V Vaccine

Around November 11, Russia’s National Research Center for Epidemiology and Microbiology, which Russia authorized for use in August ahead of even beginning a Phase III trial claimed had an efficacy rate of 92% after the second dose. It was based on a first interim analysis 21 days after the first injection during the ongoing Phase III study. On November 24, the organization claimed 95% efficacy based on new preliminary data. On December 14, 2020, they reported efficacy of 91.4%. It also offered to share one of its two human adenoviral vectors with AstraZeneca to increase the efficacy of the AstraZeneca vaccine.

Russia’s Gamaleya research institute appears to be focused on potentially marketing their vaccine worldwide. Even the name of the vaccine has emphasized the idea of a race. The organization has indicated a dose of the vaccine will cost no more than $10, about half the cost of the Pfizer vaccine. The organization has also predicted they could produce 1 billion doses in the next year. At this time, aside from Russia, it will potentially be sold in India, Korea, Brazil, China, and Hungary. The Hungarian government is the only European Union country to express interest to date.

Type: Adenovirus-based

Doses: 2

Likely EUA Date: Not applicable in the U.S.

Price: $10 per dose

Efficacy: 91.4%

Status: Early use in Russia, Emergency use Elsewhere

5. Sinovac Biotech

On January 13, 2021, China-based Sinovac Biotech reported that its COVID-19 vaccine had a 50.38% efficacy in late-stage clinical trials in Brazil. The company’s clinical trials are demonstrating dramatically varying efficacy rates. In Indonesia, a local trial demonstrated an efficacy rate of 65%, but the trial had only 1,620 participants. Turkey reported an efficacy rate of 91.25% in December 2020. Another trial in Brazil run by a local partner, Butantan Institute, reported last week a 78% efficacy rate in mild cases while 100% against severe and moderate infections. It is an inactivated vaccine that uses inactivated SARS-CoV-2 viruses.

Type: Inactivated SARS-CoV-2 virus

Doses: 2

Likely EUA Date: Not applicable in the U.S.

Price: $13,6 (Indonesia)5

Efficacy: 50.38% to 91.25%, depending on the clinical trial

Status: Approved in China, Emergency use Elsewhere

6. Johnson & Johnson

Johnson & Johnson announced on November 15 that it initiated a second global Phase III trial of its Janssen COVID-19 vaccine. They expect to enroll up to 60,000 volunteers worldwide.

Whereas all of the other three vaccine candidates require two doses about 28 days apart, the J&J vaccine only requires a single dose. Interim results from its Phase I/IIa trial demonstrated a single dose of the vaccine induced a robust immune response and was generally well-tolerated. The ENSEMBLE 2 study evaluated a two-dose regimen as well.

The vaccine uses the company’s AdVac technology platform, which it used to develop its approved Ebola vaccine and its Zika, RSV and HIV investigational vaccine candidates. It revolves around the use of an inactivated common cold virus, similar to what the AstraZeneca-University of Oxford program utilizes.

On February 4, Johnson & Johnson announced that it has filled for an emergency use authorization in the U.S. The FDA has scheduled a meeting of the committee that makes vaccine recommendations on February 26, and a decision could follow shortly afterward.  

Type: Adenovirus-based

Doses: 1

Likely EUA Date: Possibly March or April 2021

Price: $10 per dose

Efficacy: 72% in the U.S., 66% overall, 85% for preventing severe disease 

Status: Phase 3


Maryland-based Novavax makes vaccines by sticking proteins onto microscopic particles. They’ve taken on a number of different diseases this way; their flu vaccine finished Phase 3 clinical trials last March. The company launched trials for a Covid-19 vaccine in May, and the Coalition for Epidemic Preparedness Innovations invested $384 million to support research on the vaccine. In July the U.S. government awarded Novavax another $1.6 billion to support the vaccine’s clinical trials and manufacturing.

On January 28, 2021, Novavax announced that its COVID-19 vaccine, NVX-CoV2373, hit the primary endpoint with a vaccine efficacy of 89.3% in its Phase III trial in the UK. The vaccine is a protein-based COVID-19 vaccine candidate. It also has data from the South Africa Phase IIb trial and several Phase I, II and III trials. It has demonstrated high clinical efficacy against the UK and South Africa variants as well.

The vaccine contains a full-length, prefusion spike protein made using the company’s recombinant nanoparticle technology and its proprietary saponin-based Matrix-M adjuvant. It is stable at 2 to 8 degrees C and shipped in a ready-to-use liquid formulation.

Type: Protein-based vaccine

Doses: 2

Likely EUA Date: Possibly in March or February 2021 in the UK; possibly Q1 2021 or later in the U.S.

Price: $16 in the US

Efficacy: 89.3%

That’s it. The article about Coronavirus Vaccine Comparison. If you like to see another article, please follow the link below.

Also Read Delaying second dose of coronavirus vaccines is ‘risky gamble’: according to experts

Coronavirus Vaccine Comparison


  1. Carl Zimmer, Jonathan Corum, Sui-Lee Wee. Coronavirus Vaccine Comparison Tracker.2 February 2021.
  2. Gregory A.Poland, MD; Inna G. Ovsyannikova, PhD; Stephen N.Crooke. SARS-CoV-2 Vaccine Development: Current Status. 2020. Mayo Clinic. Access: 6 February 2021.
  3. WHO. Vaccines and Immunization: What is vaccination?. Access: 4 February 2021.{adgroupsurvey}&gclid=CjwKCAiA9vOABhBfEiwATCi7GA4Q0gma7eld7lLLdXFkF64O_a9BqrMusUos10__fOldtUZX9fbpfhoCpxAQAvD_BwE)
  4. Mark Terry. UPDATED Comparing COVID-19 Vaccines: Timelines, Types and Prices. Access: 4 February 2021.
  5. Milton Lum, Dr. Covid-19 Vaccine Prices. Code Blue, Health is Human Right. December 2020. Access : 16 February 2021


Pediatric Asthma And Covid-19 – Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory.


Asthma is the most prevalent chronic respiratory disease worldwide, affected people all ethnic groups throughout all ages. Asthma also the most common chronic disease in children. Asthma can’t go away, but it can be reduced to become more severe. But its still become significant public health problem. Furthermore, asthma disproportionately affects minorities and socioeconomically disadvantages children.2


From epidemiological and experimental studies shows that there is relationship between environmental factors and allergic r4espiratory disease such as rhinitis and asthma.3 Air pollution could be the reason of each asthma cases in the Asia Pacific especially in urban cities with rapid developing economics, increasing infrastructure, numbers of vehicles, and reduced green spaces. Fossil fuel and transportation are the main sources of air pollution (e.g., sulfur oxide and nitrous) released into the atmosphere leading to health problems. A global study that 9–23 million and 5–10 million annual asthma emergency room visits globally in 2015 could be attributable to O3 and particulate matter (PM) with a diameter of 2.5 μm or less (PM2.5), respectively, representing 8%–20% and 4%–9% of the annual number of global visits, respectively.3

The top 3 countries for both asthma incidence and prevalence in Asia were India, China, and Indonesia, driven largely by population size nearly half (48%) of estimated O3-attributable and over half (56%) of PM2.5-attributable asthma emergency room visits were estimated in Southeast Asia (includes India), and western Pacific regions (includes China). Of all countries globally, India and China had the most estimated asthma emergency room visits attributable to total air pollution concentrations, respectively contributing 23% and 10% of global asthma emergency room visits estimated to be associated with O3, 30% and 12% for PM2.5, and 15% and 17% for nitrogen dioxide (NO2). In this global study,16 million new pediatric asthma cases could occur globally each year due to anthropogenic PM2.5 concentrations, translating to 33% of global pediatric asthma incidence. The percentage of national pediatric asthma incidence that may be attributable to anthropogenic PM2.5 was estimated to be 57% in India, 51% in China, and over 70% in Bangladesh.3

Asthma affects 1 in 12 US children aged 0 through 17 years. After decades of increases, the prevalence of asthma in this group plateaued between 2010 and 2012, decreased in 2013 from 9.3% in 2012 to 8.3%, and remained stable through 2016. In contrast, pediatric asthma prevalence in black children increased between 2001 and 2009, leveling off by 2013. In 2016, asthma prevalence in black children rose sharply to 15.7% (a 2.3% increase from 2014 and 2015), twice that of white children. This rate surpassed that of Puerto Rican children, who previously had the highest prevalence of asthma of all US children. The prevalence of asthma in children in poverty did not decrease between 2001 and 2013 and remained high in 2016 (10.5%).2

pediatric asthma and covid
Picture 1. Asthma Prevalence in Indonesia in all ages, 2013-20184

Percentages asthma more higher  in the city than villagers

Asthma has become an issue of international development as its economic and social cost have been recognized. Asthma is one of the chronic respiratory diseases (CRDs), CRD’s ) including asthma cause 15% of world deaths. Strangely we still didn’t understand exactly what can cause number of asthma increasing each year.


  1. Microbial Exposure

Hygiene and environment have been suggested to become cause problem increasing the risk of asthma. Accordingly, children raised in modern environment with a scanty natural microbial burden may be prone to develop allergic diseases in view of an under stimulation of the immune system. Indeed, recent evidences showed that exposure to some microbes can protect from atopy, whereas others seem to promote allergic diseases. The timing of exposure to as well as the properties of the infectious agent, in addition to the genetic susceptibility of the host, may influence the future development of asthma.5

Data from the Copenhagen birth cohort first showed that infants carrying 3 major pathogenic bacteria in their nasopharynx (ie, Streptococcus pneumoniae, Moraxella catharralis, and Haemophilus influenzae) were more likely to develop asthma by the age of 6 years than those not carrying these microbes.6

2. Atopy

Word atopy originally from the Greek “atopos” meaning out of place.(William C. Shiel Jr., MD, FACP, FACR, Medical Definition of Atopy. Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens. ATOPY DEFINITION, American Academy of Allergy Asthma & Immunology). Data from epidemiological studies showed the strong link between asthma and atopy. Indeed, the family history of atopy is considered one of the most relevant risk factors for developing asthma.5Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma, atopic dermatitis (eczema) .

From a study showed that children who were sensitized to 1 or more aeroallergens by age 1 year had the highest rate of asthma at year 13. Children who were not sensitized at year 1 but sensitized to 1 or more aeroallergens by age 5 years had a 40% rate of asthma at age 13 years.7

3. Environmental Exposure

The increasing case of asthma in metropolitan areas was possibly because of their air pollution. An evidence from a study showed evidence that increased childhood exposure to PM2,5 and black carbon was associated with increased risk of asthma at age 12 years.5 According to the WHO, nearly one million of the 3.7 million people who died from ambient air pollution in 2021 lived in South-East Asia. Several areas in Indonesia such as Sumatra and Borneo island resulted in spikes of increased pollution and health hazard by produced smoke haze.3 Several studies have linked the smoke and haze produced by the fires to chronic respiratory problems.

Living in an environment where the number of smokers are high mainly can cause lung damage eventually when it happens near of children area or even to a pregnancy. Several negative effects of nicotine exposure on structural and functional development of the fetal lung were established, such as alteration of the alveolar phase, damage of the epithelial cells of type I, inhibition of fibroblast proliferation, reduction of the small airways caliber, increase of the muscular tone, and reduction of lung compliance. Exposure during pregnancy may be responsible for permanent modifications of the respiratory tract that can persist into adulthood and might culminate in chronic obstructive pulmonary disease.7


In fact, there is still no reported cases of asthma in pediatric can be the risk factor of covid-19. Children are less commonly symptomatic with coronavirus disease-2019 (COVID-19) than adults. Those who are symptomatic less commonly require hospitalization. Among 96% of cases where age was known, only 8,1% was among children less than 18 years of age. A report of 12.055 COVID-19 patients in Italy also supports a lower risk in children, although noting that COVID-19 can affect children of any age, including infants.8

Multiple international organizations including the CDC list asthma as a prognostic factor for COVID-19 outcomes such as morbidity and mortality. There is also a theoretical risk that COVID-19 could trigger viral-induced asthma exacerbations but still no data to support.   

The clinical course of COVID-19 in children is usually milder than in adults. A study stated that 23% of children with severe form of the disease have an underlying condition.9


Diagnosis of pediatric asthma and covid -19 during COVID-19 Pandemic may be complicated by a similarity in symptoms between COVID-19 (dry cough, shortness of breath) and worsening asthma. As a result, even if cough history is consistent with asthma, screening protocols for COVID-19 should be applied to all children who have worsening cough or shortness of breath, and appropriate personal protective equipment worn.8

lung function test such as spirometry is specific test for diagnosing a asthma, but in terms of COVID-19 pandemic The North American guidance on passed resumption of allergy care during COVID-19 notes that for Phase 2 rollout (community infection risk declining/stable) “spirometry is still contraindicated in most scenarios because of the aerosolization risk, except in highly individualized situations in which it would be essential for immediate treatment decision that could not otherwise be made without such information and where it can be performed with appropriate precautions and room/equipment disinfection.8

  • What is parents have to know if their kids develop an asthma during this Corona Virus pandemic?

Differentiating COVID-19 from worsening asthma, or an asthma exacerbation, is challenging. As a result, pediatricians and families have an essential role in ensuring that children with asthma maintain good asthma control during this time.10

Multiple international guidelines support children with asthma remaining on their maintenance asthma medications, such as inhaled corticosteroids or antileukotrienes, during COVID-19 if they are well controlled. A statement from the European Academy of Allergy Asthma and Clinical Immunology (EAACI) notes that “since asthma itself may be a risk factor for the severity of COVID‐19 disease and since the use of ICS does not pose an increased risk for pulmonary or systemic infections in children with asthma, their regular use is unlikely to increase the risk of acquiring the infection or increasing the severity of the present infection.8

Children and adolescents with asthma should remain on their current asthma medications and still practice social distancing and make sure to avoid aeroallergen also exposure to second-hand cigarette smoking10, because it can increase the expression of the ACE2 receptors in the lower respiratory tract, which is the coronavirus receptor. Which ACE2 as the receptor for Sars-CoV-2 means it will increase susceptibility to contract the COVID-19 infection and potentially to develop a more severe form.8

pediatric asthma and covid


  1. GINA committees. POCKET GUIDE FOR ASTHMA MANAGEMENT AND PREVENTION for adults and children older than 5 years.2019. Access :
  2. Shilpa J. Patel, MD,MPH, Stephen J. Teach, MD, MPH. Asthma. Pediatrics in Review, An Official Journal of the American Academy of Pediatrics. Vol 40 No II November 2019. Division of Emergency Medicine, Children’s National Medical Center, Washington, DC. Access :
  3. Ruby Pawankar, Jiu-Yao Wang, I-Jen Wang, Francis Thien. White Paper 2020 on Climate Change, Air Pollution, and Biodiversity in Asia-Pacific and Impact on Allergic Disease. Asia Pacific Association of Allergy, Asthma and Clinical Immunology. 2020. Jan;10(1):e11. Access :
  4. Kementerian Kesehatan RI. Hasil Utama RISKESDAS 2018. Penyakit Tidak Menular, Prevalensi Asma. Access :
  5. Giuliana Ferrante and Stefania La Grutta. The Burden of Pediatric Asthma. Frontiers in Pediatric. June 2018. Volume 6. Article 186. Access : Frontiers | The Burden of Pediatric Asthma | Pediatrics (  
  6. Fernando D. Martinez, MD. Childhood Asthma Inception and Progression Role of Microbial Exposures, Susceptibility to Viruses and Early Allergic Sensitization. Elsevier Ltd. Volume 39, Issue 2. 2019. P 141-150. Access : Childhood Asthma Inception and Progression: Role of Microbial Exposures, Susceptibility to Viruses and Early Allergic Sensitization – ScienceDirect
  7. Frederick J. Rubner, MD, Daniel J. Jackson, MD, Michael D. Evans, MS. Early life rhinovirus wheezing, allergic sensitization, and asthma risk at adolescence. 2017. The Journal of Allergy and Clinical Immunology. Asthma and Lower Airway Disease. Volume 139, issue 2, P501-507. Early life rhinovirus wheezing, allergic sensitization, and asthma risk at adolescence – Journal of Allergy and Clinical Immunology (
  8. Elissa M.Abrams MD, FRCPC. Ian Sinha MBBS, FRCPCH, PhD. Pediatric Asthma and COVID-19: The known, the unknown, and the controversial. Wiley Periodicals LLC: Pediatric Pulmonology. 2020; 55:3573-3578. DOI: 10.1002/ppul.25117
  9. M. Kamali Aghdam, M. Sadeghzadeh, S. Sadeghzadeh and K. Namakin. Challenges in A Child with Asthma and COVId-19. Elsevier Ltd. 2020. New Microbe and new Infections, Vol 37 Number C. Access : Challenges in a child with asthma and COVID-19 – ScienceDirect
  10. Elissa M. Abrams, MD, MPH, and Stanley J. Szefler, MD. Managing Asthma during Coronavirus Disease-2019: An Example for Other Chronic Conditions in Children and Adolescents. The Journal of Pediatrics. Vol 222. July 2020. Access:


I have Diabetes, should I go for COVID-19 vaccination?

Covid-19 and Diabetes – In December 2019, a novel coronavirus, SARS-CoV-2, was identified as the pathogen  causing coronavirus disease (COVID-19) in Wuhan, China (11, 51, 55). On March 11, 2020, COVID-19 was declared a pandemic  by the World Health Organization. As of March 27, 2020, there have been a total of 103,942 confirmed cases with 1689 deaths in the United States. Globally, 27,324 deaths have been reported among 595,800 confirmed cases.

On 21st January 2021 there have been 95,612,831 confirmed cases of COVID-19, including 2,066,176 deaths, reported to WHO. As of January 2021, there have been 24.037.236 confirmed cases in the United States, 3.505.758 confirmed cases in the United Kingdom, 951.651 confirmed cases in Indonesia.

In 2019, approximately 463 million adults (20-79 years) were living with diabetes; by 2045 this will rise to 700 million. The proportion of people with type 2 diabetes is increasing in most countries 79% of adults with diabetes were living in low- and middle-income countries. 1 in 5 of the people who are above 65 years old have diabetes. 1 in 2 (232 million) people with diabetes were undiagnosed. Diabetes caused 4.2 million deaths. Diabetes caused at least USD 760 billion dollars in health expenditure in 2019 – 10% of total spending on adults. More than 1.1 million children and adolescents are living with type 1 diabetes. More than 20 million live births (1 in 6 live births) are affected by diabetes during pregnancy, 374 million people are at increased risk of developing type 2 diabetes.

Also Read Things People With Diabetes Must Know About the COVID-19 Vaccines

Diabetes is a serious threat to global health that respects neither socioeconomic status nor national boundaries. People living with diabetes are at risk of developing a number of serious and life-threatening complications, leading to an increased need for medical care, a reduced quality of life, and undue stress on families. Diabetes and its complications, if not well managed, can lead to frequent hospital admissions and premature death. Globally, diabetes is among the top 10 causes of death.

Source : Pusdatin Figure 1. Prevalence of Diabetes age 20-79 in 2019
covid-19 and diabetes
Source Pusdatin Figure 2. Top 10 countries with highest Diabetes in 2019

The genetic sequence of SARS-CoV-2 showed more than 80% shared identity to SARS-CoV and 50% to the MERS-CoV, and both SARS-CoV and MERS-CoV originate in bats and infect humans and wild animals. CoV is made up of four structural proteins: spike (S), membrane (M), nucleocapsid (N), and envelope (E) proteins. The S protein mediates receptor binding on the host cell membrane through the receptor-binding domain (RBD) in the S1 domain and membrane fusion through the S2 subunit. Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV and SARSCoV-2, in contrast to MERS-CoV, which utilizes dipeptidyl peptidase 4 (DPP4) as its cellular receptor. This interaction thus determines host tropism and ultimately clearance of the virus. ACE2 is expressed in the upper respiratory system, type I and II alveolar epithelial cells in the lungs, the heart, endothelial cells, kidney tubular epithelium, enterocytes, and the pancreas. After binding to ACE2, proximal serine proteases such as TMPRSS2 are involved in S protein priming and cleavage of the spike. Proteases such as Furin subsequently release the spike fusion peptide, and the cellular virus enters through an endosomal pathway . The low pH and presence of proteases such as cathepsin-L  characteristic of the endosomal micro environment favor the delivery of SARS-CoV-2 genome into the cytosol  where further viral replication leads to the formation of mature virions and subsequent spread. Infected cells undergo apoptosis  or necrosis  and trigger inflammatory responses marked by the activation of proinflammatory cytokines or chemokines, which leads to the recruitment of inflammatory cells. CD4+ T helper (Th1) cells regulate antigen presentation and immunity against intracellular pathogens such as CoV through interferon gamma (IFN-ℽ) production. Th17 cells induce the recruitment of neutrophils and macrophages by producing interleukin-17 (IL-17), IL-21, and IL-22. SARS-CoV-2 infects circulating immune cells and increases apoptosis of lymphocytes (CD3, CD4, and CD8 T cells), leading to lymphocytopenia. Indeed, the degree of lymphocytopenia is associated with the severity of SARS CoV-2 infection. Lower T cell function relieves the inhibition on innate immune system leading to secretion of high amounts of inflammatory cytokines in what is known as a cytokine storm. In fact, circulating levels of cytokines/chemokines [IL-6, tumor necrosis factor-α (TNF)] and chemokines [CXC-chemokine ligand 10 (CXCL10) and CC-chemokine ligand 2 (CCL2)] involved in the cytokine storm syndrome are elevated and may play a role in SARSCoV-2-driven hyperinflammation leading to multiorgan failure.

Potential mechanisms that increase the risk of COVID-19 in diabetes. It is now well recognized that older age and the presence of diabetes, hypertension, and severe obesity (BMI =40 kg/m2 ) increase morbidity and mortality in patients with COVID-19. Considering the high prevalence of cardiovascular disease (CVD), obesity, and hypertension in patients with diabetes, it is unknown whether diabetes independently contributes to this increased risk. However, plasma glucose levels and diabetes are independent predictors for mortality and morbidity in patients with SARS. Potential mechanisms that may increase the susceptibility forCOVID-19 in patients with diabetes include: 1) higher affinity cellular binding and efficient virus entry, 2) decreased viral clearance, 3) diminished T cell function, 4) increased susceptibility to hyperinflammation and cytokine storm syndrome, and 5) presence of CVD. Augmented ACE2 expression in alveolar AT2 cells, muscle of the heart, kidney, and pancreas may favor increased cellular binding of SARS-CoV-2. Increased expression of ACE2 has been demonstrated in the lung, kidney, heart, and pancreas in rodent models of diabetes. Insulin  administration attenuates ACE2 expression, while hypoglycemic agents such as glucagon-like peptide-1 (GLP-1) agonists (liraglutide) and thiazolidinediones (TZDs; pioglitazone), antihypertensives such as ACE inhibitors, and statins upregulate ACE2. Until recently, whether diabetes was causally linked to ACE2 expression levels in the lung in humans was unknown.

covid-19 and diabetes
Source :

Fig. 3. Cellular entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The initial step in cellular entry of the virus is the binding of SARS-CoV-2 spike protein to cell surface angiotensin converting enzyme 2 (ACE2). Cellular proteases such as TMPRSS2 and furin are involved in priming of the S protein, which involves cleavage at the S1/S2 domains. This allows the fusion of the virus to the cell surface. Virions are taken up into endosomes, where SARS-CoV-2-S is cleaved and possibly activated by the pH-dependent cysteine protease cathepsin L. Once inside the cell, SARS-CoV-2 uses the endogenous cellular machinery to replicate itself. ACE catalyzes the conversion of angiotensin(Ang)ItotheoctapeptideAngII,whereasACE2 converts Ang II to Ang1–7. AngII through the activation of Ang II type 1a receptors induces vasoconstriction and proliferation,whereasAng1–7 stimulates vasodilatation and suppresses cell growth.

covid-19 and diabetes
Source :

Fig. 4. Putative mechanisms contributing to increased susceptibility for coronavirus disease (COVID-19) in patients with diabetes mellitus (DM). Following aerosolized uptake of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), invasion of the respiratory epithelium and other target cells by SARS-CoV-2 involves binding to cell surface angiotensin converting enzyme 2 (ACE2). Increased expression of ACE2 may favor more efficient cell binding and entry into cells. Early recruitment and function of neutrophils and macrophages are impaired in DM. Delay in the initiation of adaptive immunity and dysregulation of the cytokine response in DM may lead to the initiation of cytokine storm.

            There is a paucity of data in the world (including Indonesia) regarding comorbidities and COVID-19 outcomes and mechanism that modulate viral pathogenesis. But here is our mainly concern that people with comorbidities likely have chance to get COVID-19, so its mainly our concern that people with Diabetes should get vaccinated.

Several clinical reports have described greater morbidity and mortality from COVID-19 in people with diabetes, often accompanied by obesity. Most of this information is from individuals with type 2 diabetes, with less known about the risk in type 1 diabetes, a phenotypically distinct disorder. Experts have cautioned against extrapolating from studies of type 2 diabetes to individuals with type 1 diabetes. In the USA, the Centers for Disease Control and Prevention (CDC) currently categorize type 1 and type 2 diabetes differently in terms of risk for severe illness from COVID-19, with people with type 2 diabetes considered “at increased risk for severe illness” and those with type 1 diabetes categorized as “might be at increased risk”. Importantly, several recent studies have shown that both people with type 2 diabetes and those with type 1 diabetes have an increased vulnerability to serious illness from SARS-CoV-2 compared with people without diabetes. In relative terms, patients with type 1 diabetes and those with type 2 diabetes had similar adjusted odds ratios (ORs) for hospitalization (3·90 for type 1 diabetes vs 3·36 for type 2 diabetes), severity of illness (3·35 vs 3·42), and in-hospital mortality (3·51 vs 2·02). In a population-based study in Scotland, the risk of fatal or critical care unit treated COVID-19 was increased for both diabetes types (OR 2·4 with type 1 diabetes vs 1·4 with type 2 diabetes).


Abbreviation: COVID-19 = coronavirus disease 2019.

* Data sources for each group: health care personnel (American Community Survey, 2019; ); long-term care facility residents (Minimum Data Set. Centers for Medicare & Medicaid Services; ); frontline and other essential workers (American Community Survey, 2019; ); age-specific groups (U.S. Census; ); high-risk medical conditions (Behavioral Risk Factors Surveillance System, 2018; ).

† Excludes persons who were recommended to receive vaccine in an earlier phase (e.g., persons aged 65–74 years who are living in long-term care facilities or who are health care personnel, who would have been included in Phase 1a) and accounting for overlap between groups within the same phase (e.g., essential workers with high risk medical conditions).

§ Estimates for frontline and other essential workers are approximate and derived from prepandemic survey data; relative proportions will vary by state.

¶ As of December 18, only the Pfizer-BioNTech COVID-19 vaccine is authorized for use in persons aged 16–17 years.

            Based on ongoing review of the literature, CDC has identified medical conditions or risk behavior that are associated with increased risk for severe COVID-19. The risk for COVID-19 associated hospitalization increases with the number of high-risk medical conditions, from 2,5 times the risk for hospitalization for person with one condition to 5 times the risk for those with three or more conditions.

            As we can see from the table above that Person aged 65-74years and Person aged 16-64years with high-risk medical conditions are included in Phase 1c to receive COVID-19 vaccine. So we conclude that person with diabetes are included in Phase 1c.

Indonesian Society of Internal Medicine(PAPDI) made the recommendations regarding COVID-19 vaccination (Sinovac) in patients with concomitant disease/comorbidities. People with diabetes are included to get vaccination which they described it all patient with controlled type 2 diabetes and HbA1C below 58 mmol/mol or 7,5%, vaccine can be given.


  1. Ranganath Muniyappa and Sriram Gubbi. 2020. COVID-19 pandemic, coronaviruses, and diabetes melitus. American Physiological Society. doi:10.1152/ajpendo.00124.2020
  2.,22 January). WHO Coronavirus Disease (COVID-19) Dashboard.
  3.,22 January). COVID 19.
  4., 21 January). Internatinal Diabetes Federation: About Diabetes.
  5., 21 January). Diabetes Melitus-Kementerian Kesehatan.
  6. Kathleen Dooling, MD, Mona Marin, MD, Megan Wallace, DrPH. 2021. The Advisory Committee on Immunization Practices’ Updated Interim Recommendation for Allocation of COVID-19 Vaccine -United States, December 2020. US Department of Health and Human Services/Centers for Disease Control and Prevention: Morbidity and Mortality Weekly Report. Vol.69, No.51-52.
  7. Alvin C POwers, David M Aronoff, Robert H Ecked. 2021. COVID-19 vaccine prioritization for type 1 and type 2 diabetes. The Lancet Diabetes Endocrinal 2021. S2213-8587(21)00017-6
  8., 22 January). Rekomendasi PAPDI tentang Pemberian Vaksinasi COVID-19.

Seasonal Affective Disorder “Winter Blues”

Seasonal Affective Disorder “Winter Blues”

Seasonal Affective Disorder – Depression is one of the mental health problems that can affect people around the world. Mental health is a major issue for adolescents. WHO said up to half of mental health conditions start before the age of 14. Poor mental health is the leading cause of disability in young people, and accounts for a large proportion of the global disease burden during adolescence. Suicide is third leading cause of death in 15-19 years-old.1

Also Read Things People With Diabetes Must Know About the COVID-19 Vaccines


Seasonal affective disorder is a form of depression also known as SAD, seasonal depression or winter depression.2. Many people may experience mood changes begin and end when the seasons change.

In most cases, SAD symptoms start in the late fall or early winter and go away during the spring and summer; this is known as winter-pattern SAD or winter depression. Some people may experience depressive explodes during the spring and summer months; this is called summer-pattern SAD or summer depression and is less common. The occurrence and nature of seasonal rhythms in humans has received renewed interest since Seasonal Affective Disorder (SAD) was diagnosed in 1984.3(SAD Endocrinology journal)

An estimated 10 to 20 percent of recurrent depression cases follow a seasonal pattern. Although a summer pattern of recurrence is possible, the predominant pattern involves fall/winter depression with spring/summer remission. In U.S. community surveys, SAD prevalence ranges from 9.7 percent in New Hampshire to 1.4 percent in Florida. In North America, SAD prevalence increases with latitude, but the correlation is nonsignificant in other parts of the world.4(SAD Overview journal)

Symptoms  (SAD from NIH)

SAD is not considered a separate disorder but is a type of depression characterized by its recurrent seasonal pattern. Therefore, the signs and symptoms of SAD include those associated with major depression, and some specific symptoms that differ for winter-pattern and summer-pattern SAD. Not every person with SAD will experience all of the symptoms listed below.

Symptoms of major depression may include: 

● Feeling depressed most of the day, nearly every day

● Losing interest in activities you once enjoyed

● Experiencing changes in appetite or weight

● Having problems with sleep

● Feeling sluggish or agitated

● Having low energy

● Feeling hopeless or worthless

● Having difficulty concentrating

● Having frequent thoughts of death or suicide

For winter-pattern SAD, additional specific symptoms may include:

● Oversleeping (hypersomnia)

● Overeating, particularly with a craving for carbohydrates

● Weight gain

● Social withdrawal (feeling like “hibernating”)

Specific symptoms for summer-pattern SAD  may include:

● Trouble sleeping (insomnia)

● Poor appetite, leading to weight loss

● Restlessness and agitation

● Anxiety

● Episodes of violent behavior

How is SAD Happen?

Many studies shows there are connection between the season changes and hormonal level in human body, especially hormone that arrange human’s mood like serotonin and melatonin  which is work to maintain our sleep-wake cycle. But pathogenic theories for SAD have focused on neurotransmitters, hormones, circadian rhythm dysregulation, genetic polymorphism, and psychological factors.(SAD overview).

One of first hypothesis about SAD was that the shorter winter photoperiod (light-dark cycle) led to depressive symptoms. A melatonin hypothesis in SAD explained in many animals, the photoperiod signal is mediated by the duration of nocturnal melatonin secretion, and light suppresses melatonin secretion.   However, the 24-hour melatonin rhythm in winter was no different between SAD patients and controls, and did not change with light treatment. Melatonin suppression alone is also not enough to produce a therapeutic response. Recent studies, however, have revived the photoperiod hypothesis. The nocturnal duration of melatonin secretion reflects changes in the photoperiod in humans. In normal subjects in naturalistic living conditions, no changes in melatonin profiles were found between summer and winter, suggesting that artificial indoor light may suppress the melatonin response to seasonal changes in photoperiod.

The phase-shift hypothesis proposes that the body’s sleep-wake cycle is phase-delayed in SAD with respect to the environmental light dark cycle, and is based on observations of delayed onset of sleep, melatonin, body temperature, and cortisol rhythms in some SAD patients. Individuals with SAD may respond to longer nights in winter with an extended duration of nocturnal melatonin release, a hormone that can promote sleep. When measuring active melatonin secretion under constant dim light, Wehr, et al.,21 found that individuals with SAD had a longer duration of melatonin release during winter than summer whereas controls did not. This is analogous to the lengthened duration of melatonin release in some mammals that signals seasonal changes in reproductive activity. It is possible that only humans with SAD have retained the ability to track seasons in this way, which might explain the seasonal presentation of SAD. Recent etiological models have attempted to integrate biological and psychological mechanisms in explaining SAD onset and maintenance. Young’s dual vulnerability model proposes two separate vulnerabilities among individuals with history of SAD: 1) a physiological vulnerability to experience atypical symptoms during the winter and 2) a psychological vulnerability to develop cognitive and affective symptoms of depression in reaction to the vegetative symptoms. Young devised this hypothesis based on his finding that individuals with SAD retrospectively recounted onset of fatigue, hypersomnia, and increased appetite prior to developing cognitive and affective symptoms. Different pathophysiological mechanisms may account for the different vulnerabilities proposed, leading to heterogeneity of findings from studies addressing the etiology and treatment of SAD.

In a phase-delay hypothesis, morning light therapy is predicted to be superior to evening light because morning light exposure results in a corrective phase-advance, while evening light exposure should further delay the circadian phase. Light exposure in the middle of the day generally has no effect on circadian rhythms, and hence should have no therapeutic effect. Initial studies used the dim-light melatonin onset (DLMO, the time that melatonin begins to be secreted by the pineal gland during controlled, dim-light conditions) as a marker of circadian phase because it is relatively free of masking effects. Patients with SAD were found to have phase-delayed DLMO compared with control subjects; furthermore, morning light exposure resulted in phase advances, while evening light exposure resulted in phase delays, and only the morning exposure led to clinical improvement.(pathopisiology of SAD journal)

Can SAD be cure?

Yes, it can be cured. Therefore, it needs a holistic treatment plan. Not only medication, but each area that contribute to be the cause of SAD must be treated as well. Treatments are available that can help many people with SAD. There are three main categories of the therapy :

  1. Light Therapy

Since the 1980s, light therapy has been a mainstay for the treatment of SAD. It aims to expose people with SAD to a bright light every day to make up for the diminished natural sunshine in the darker months.

For this treatment, the person sits in front of a very bright light box (10,000 lux) every day for about 30 to 45 minutes, usually first thing in the morning, from fall to spring. The light boxes, which are about 20 times brighter than ordinary indoor light, filter out the potentially damaging UV light, making this a safe treatment for most. However, people with certain eye diseases or people taking certain medications that increase sensitivity to sunlight may need to use alternative treatments or use light therapy under medical supervision. (Journal from NIH). A pooled analysis of light therapy studies 40 concluded that 53.3 percent of individuals with SAD met criteria for full remission with light therapy. However, only 43 percent of individuals with moderate to severe SAD symptoms remitted with light therapy. (SAD overview)

  • Antidepressant’s Drugs

SAD was mainly perform the major depression symptoms that its associated with disturbances in serotonin activity, antidepressant medications called selective serotonin reuptake inhibitors (SSRI’s) are also used to treat SAD when symptoms occur.

Clinically, antidepressants drugs are frequently used as an alternative to light therapy. (sad overview). Five-center Canadian study found comparable remission rates for light therapy plus pill placebo (54%) and fluoxetine  plus dim light placebo (50%). In a retrospective analysis of SAD outpatients in Finland, 73% of eight patients treated with moclebemide and 61 percent of 11 patients treated with fluoxetine responded over 6 weeks. Eight women with SAD due to randomized study had combined light therapy and citalopram or light therapy or light therapy and placebo found no difference in the two conditions at post-treatment, but greater efficacy for combination treatment 34 weeks later. (SAD overview)

  • Cognitive Behavioral Therapy

The CBT for SAD protocol involves 90 minutes sessions twice a week over six weeks (total of 12 sessions) delivered in group format. The behavioral component uses pleasant activity scheduling to counteract “hibernation” by developing wintertime interests. Negative cognitions are identified and challenged, including thoughts related to winter, light availability, seasonal environmental cues, and weather. Relapse-prevention emphasizes using CBT skills during subsequent fall/winter seasons in response to anticipatory negative thoughts about winter or SAD-related behavior changes.


Exercise and light therapy were associated with similar and significant reductions in depression severity and an increased rate of oxygen consumption relative to an untreated control group, suggesting that normalization of daily energy expenditure may underlie the efficacy of both treatments. Although morning exercise might be beneficial in the treatment of SAD, based on the assumption that it would induce a phase advance, these results suggest that the timing of exercise may not be important to the antidepressant effects of exercise on SAD. However, exercise late at night might be contraindicated in SAD because it can lead to a phase delay in the onset of melatonin release the following night in humans.56 In healthy controls, aerobic exercise performed under bright (2,500- to 4,000-lux) lights appears to be more beneficial than either exercise under typical indoor lighting or no exercise for atypical symptoms and vitality.


  1. New WHO guidelines on promoting mental health among adolescents.
  2. Felix Torres, M.D., MBA, DFAPA. Seasonal Affective Disorder. American Psychiatric Association.
  3. Seasonality in Affective Disorders. Anna Wirz-Justice. 2017. General and Comparative Endocrinology
  4. Kathryn A. Roecklein, Kelly J.Rohan, PhD. Seasonal Affective Disorder. 2005. Department of Medical and Clinical Psychology, Uniformed Services University of the Health Science in Bethesda,Maryland.
Things People With Diabetes Must Know About the COVID-19 Vaccines

Things People With Diabetes Must Know About the COVID-19 Vaccines

Things People With Diabetes
Source : Everydayhealth

People with diabetes are at a higher risk of developing complications of COVID-19, making it all the more important that they are vaccinated against the disease as soon as possible.

It’s a new year, and COVID-19 vaccines offer hope for those wanting to protect themselves, especially people with underlying health conditions such as diabetes.

You may have questions about these new vaccines, including when you can get them and what questions you should ask your doctor about them. Experts we talked with say the vaccines are safe, effective, and important for people with diabetes.

“The most important thing is that people with diabetes get vaccinated as soon as it becomes available to them,” says Robert Gabbay, MD, PhD, chief science and medical officer for the American Diabetes Association (ADA) in Arlington, Virginia.

Also Read Covid-19 Vaccine Updates

1. When Will I Be Able to Get the Vaccine if I Have Diabetes?

It depends on where you live. At a federal level, the Centers for Disease Control (CDC) makes recommendations about who should receive priority for vaccination. It is then up to each state to use those recommendations to plan for and distribute vaccines to counties and residents.

Even so, guidelines are changing. In mid-January, U.S Health and Human Services (HHS) Secretary Alex Azar said Americans 65 years and older and those who are younger but have underlying health conditions should receive priority, as AARP reports.

If your state is following the CDC’s recommendations, healthcare workers and nursing home residents are receiving first priority for the vaccine. Next, the CDC recommends vaccinating frontline workers such as firefighters, teachers, and grocery store workers, along with people over 75.

Then, the CDC recommends vaccinating people with type 2 diabetes and other underlying medical conditions due to their increased risk of severe COVID-19-associated illness.

People with type 1 diabetes do not currently have the same priority vaccination with the CDC. But groups including the Juvenile Diabetes Research Foundation (JDRF) and the ADA are advocating for this priority at a federal and state level.

Justin Gregory, MD, assistant professor of pediatrics at Vanderbilt Children’s Hospital in Nashville, who has type 1 diabetes, says that people with type 1 diabetes should have the same priority for vaccination as people with type 2 diabetes because both groups have a similarly increased risk for dangerous and deadly COVID-19 illness. 

In the end, states make their own decisions about vaccination priority, so check your state and local health department’s website to find out when you are eligible. The ADA has also assembled links to individual states’ vaccination plans as part of its COVID-19 Vaccination Guide.

2. Does Having Another Health Condition With Diabetes Affect My Place in Line?

Potentially. The CDC notes notes that the risk for hospitalization increases with the more “high-risk” medical conditions a person has — it’s 2.5 times for a person with one condition and 5 times for people with three or more conditions. Nevertheless, having comorbidities, such as heart and kidney disease, does not mean you will be allowed to get vaccinated before someone with only diabetes or another single health condition. Again, it comes down to where you live.

In Massachusetts, for example, people with two or more underlying conditions are prioritized to get a COVID-19 vaccine before those with only one condition. Other states do not designate priority by the number of underlying medical conditions.

3. Are COVID-19 Vaccines Free for People With Diabetes?

The COVID-19 vaccine is free for everyone, regardless of diabetes status, according to the CDC. However, some providers administering the vaccine may charge a fee, which can be reimbursed by your public or private health insurance, or by the Health Resources and Services Administration’s Provider Relief Fund if you do not have insurance.

4. Why Is It Important to Get the Vaccine if You Have Diabetes?

“It’s quite clear that people with diabetes do much worse than people without diabetes in terms of their outcomes with COVID,” says Dr. Gabbay. Early in the pandemic, a study from the CDC found that roughly half of people who died from COVID-19 under age 65 had diabetes. 

The protective effects of vaccines are critical for people with diabetes who are at increased risk for severe and deadly infection from COVID-19, says Dr. Gregory. His December 2020 study in Diabetes Care found that people with type 1 or type 2 diabetes are 3 times more likely to be hospitalized or experience severe COVID-19 illness compared with people without diabetes. 

Two studies from the United Kingdom showed similar risk. An October 2020 study in The Lancet Diabetes & Endocrinology found that people with type 1 or type 2 diabetes were 2 to 3 times more likely to die from COVID-19 in the hospital than people without diabetes. And a December 2020 study in The Lancet Diabetes & Endocrinology found that people with type 1 or type 2 were more likely to die or to be treated in the intensive care unit for COVID-19.

5. Are the Vaccines Safe and Effective for People With Diabetes?

Two COVID-19 vaccines are currently available in the United States — and people with diabetes were included in both the vaccine trials. Both require two doses spaced either 21 days (Pfizer-BioNTech vaccine) or 28 days (Moderna vaccine) apart. With their two doses completed, these vaccines are over 90 percent effective and received emergency use authorization from the U.S. Food and Drug Administration (FDA) in December 2020.

“We wanted to make sure we recruited a number of individuals who had the types of underlying medical conditions that can make COVID more severe,” says C. Buddy Creech, MD, MPH, director of the Vanderbilt Vaccine Research Program in Nashville and part of the phase 3 trials of the Moderna COVID-19 vaccine.

That included people with diabetes, hypertension, and obesity, says Dr. Creech. People with type 1, type 2, and gestational diabetes were included in the Moderna clinical trial, he adds. The FDA filing from Pfizer-BioNTech says the trial included but does not specify among types.

The vaccines were well-tolerated, highly efficacious, and elicited an immune response in people with underlying conditions, such as diabetes, says Creech.

“People with diabetes are going to be prioritized [for COVID-19 vaccination] because we know they’re at increased risk for disease. And they should feel confident that someone a whole lot like them was enrolled in the clinical trial so that we can say with a greater degree of certainty that they can effectively get this vaccine,” says Creech.

Gabbay says that the data do not suggest the COVID-19 vaccines pose particular risk for people with diabetes. He also says there is no reason to think there would be interactions with insulin or other medications that people with diabetes might take.

6. What Side Effects of the Vaccine Should People With Diabetes Pay Attention To?

In general, the most common side effects of both vaccines are pain, swelling, and redness at the injection site. Other common side effects are chills, tiredness, and headaches. Most of these side effects were mild, but some people had more severe reactions that interfered with daily activities.

Gabbay says side effects of the COVID-19 vaccines are similar to those of flu vaccines. For someone living with diabetes, keeping a sick-day kit with extra medications and supplies is beneficial in case you do not feel well.

7. What Questions Should People With Diabetes Ask Their Healthcare Teams About the COVID-19 Vaccines?

Gabbay says the first question patients should ask their providers about the COVID-19 vaccine is, “When can I get it?”

Be proactive in calling your provider to ask for the vaccine, says Gabbay. Check the websites of your state and local health departments to find out about local vaccine distribution. “Being patient, persistent, and informed is the best approach,” says Gabbay.


  2. By Kate Ruder Medically Reviewed by Justin Laube, MD

How Effective is a Single Vaccine Dose Against Covid-19 ?

How Effective is a Single Vaccine Dose Against Covid-19 ?

Single Vaccine Dose, How Effective it is ? – The cases are already beginning to emerge.

When 85-year-old Colin Horseman was admitted to Doncaster Royal Infirmary in late December, it was for a suspected kidney infection. But not long afterwards he caught Covid-19 – at the time, roughly one in four people in hospital with the virus had acquired it there. He developed severe symptoms and was eventually put on a ventilator. A few days later, he died.

At first glance, Horseman’s situation may seem fairly typical, though no less tragic for it. After all, at least 84,767 people have now succumbed to the disease in the UK alone at the time of writing. But, as his son recently explained in a local newspaper, less than three weeks earlier he had been among the first people in the world to receive the initial dose of a Covid-19 vaccine – the Pfizer-BioNTech version. He was due to receive the second dose two days prior to his death.

In fact, most vaccines require booster doses to work.

Take the MMR – measles, mumps and rubella – vaccine, which is given to babies around the world to prevent these deadly childhood infections. Around 40% of people who have received just one dose are not protected from all three viruses, compared to 4% of those who have had their second. People in the former group are four times more likely to catch measles than those in the latter – and there have been outbreaks in places where a high proportion of people have not completed the full MMR vaccination schedule.  

“The reason that people are so keen on boosters and consider them so vital is that they kind of send you into this whole other kind of fine-tuning mode of your immune response,” says Danny Altmann, professor of immunology at Imperial College London.

Also Read Covid-19 Vaccine Updates

How Booster Vaccines Work

When the immune system first encounters a vaccine, it activates two important types of white blood cell. First up are the plasma B cells, which primarily focus on making antibodies. Unfortunately, this cell type is short-lived, so although your body might be swimming in antibodies within just a few weeks, without the second shot this is often followed by a rapid decline.

Then there are the T cells, each of which is specifically tailored to identify a particular pathogen and kill it. Some of these, memory T cells, are able to linger in the body for decades until they stumble upon their target – meaning immunity from vaccines or infections can sometimes last a lifetime. But crucially, you usually won’t have many of this cell type until the second meeting. 

The booster dose is a way of re-exposing the body to the antigens – the molecules on pathogens that trigger the immune system. “So, once you’ve had your boost you’ll have a higher frequency of memory T cells and ditto to some extent for the size of the pool of memory B cells you’ll have. They’ll also be making higher quality antibodies.”

On second exposure to the same vaccine or pathogen, the B cells that remain from before are able to rapidly divide and create a menacing throng of descendants, leading to a second spike in the amount of antibodies circulating.

The second dose also initiates the process of “B cell maturation”, which involves selecting the immature ones with the best receptors for binding to a particular pathogen. This happens while they’re still in the bone marrow – where white blood cells are made – and afterwards they travel to the spleen to finish developing. This means B cells are not only more numerous afterwards, but the antibodies they produce are better targeted.

Memory T cells, meanwhile, also proliferate rapidly. They’re already thought to have played a critical role during the current pandemic, protecting some people from developing severe Covid-19. Though the virus may have only been circulating globally since around December 2019, there’s some evidence they may have “seen” other coronaviruses before, such as those that cause the common cold – allowing them to recognize Covid-19.



Delaying second dose of coronavirus vaccines is ‘risky gamble’: according to experts

Delaying second dose of coronavirus vaccines is ‘risky gamble’: according to experts

Delaying second dose of coronavirus vaccines is ‘risky gamble’: according to experts

Amid shortages in coronavirus vaccine supplies, some Canadian provinces have decided to delaying second dose of coronavirus, which experts have called a “risky approach” and “a gamble.”

Ontario’s government announced on Saturday that long-term care residents, staff and essential caregivers who have received their first doses of the Pfizer-BioNTech vaccine will now get the second jab within 21 to 27 days. Everyone else will receive their second dose after three weeks but before 42 days.

The time span between doses specified by Pfizer and BioNTech is 21 days.

This comes in the wake of a temporary delay in shipments of the Pfizer vaccine to Canada as the company is scaling up its European manufacturing capacity.

Last month, British Columbia said it was changing its second-dose schedule for both Pfizer and Moderna’s vaccines to 35 days to allow giving the first doses to as many people as possible right away. Moderna’s second booster shot is supposed to follow the first by 28 days.

Meanwhile, Quebec is pushing the time between the two doses to a maximum of three months in an attempt to vaccinate more seniors faster with a first injection.

These timeline changes have raised concerns and questions about the impact this may have on the effectiveness of the vaccines.

“There is a risk in this approach,” said Dr. Alberto Martin, professor of immunology at the University of Toronto.

It’s possible that a large fraction of these individuals will not develop full immunity and thereby waste many of these doses,” he told Global News.

While there is a buffer and wiggle room for a few days and weeks between vaccine doses, experts have cautioned against significant delays that deviate from the prescribed time period used in the clinical trials.

“The longer you spaced that interval, the higher risk (of) … maybe not getting the full immune response possible,” said Dr. Zain Chagla, an infectious diseases physician at St. Joseph’s Healthcare in Hamilton, in an interview with Global News.

However, since this is an experiment with no sufficient data, it still remains unclear what the exact impact of the delay will be, both Chagla and Martin said.

The World Health Organization (WHO) has advised that in case of shortages in vaccine supplies, the second Pfizer dose can be extended to up to six weeks or 42 days after the first, which is what Canada’s National Advisory Committee on Immunization (NACI) has also recommended.

Currently, there is no data on the maximum interval between doses or on medium- or long-term efficacy of COVID-19 vaccines, according to NACI.

NACI experts say delaying second dose of coronavirus up to six weeks, instead of three or four, could more quickly get at least some protection against COVID-19 to more people.

The United Kingdom, where a new, more contagious variant of COVID-19 began spreading last month, has gone against the advice of the drugmakers, as well as WHO, and delayed the second dose of Pfizer and AstraZeneca’s vaccine by up to 12 weeks.

The United States, meanwhile, is taking a different approach and sticking with the originally specified timeframe of 21 days between Pfizer’s shots and 28 days for Moderna.

In a statement on its website, the U.S. Food & Drug Administration says changes in the schedules of vaccine administration without appropriate supporting data can pose a “significant risk of placing public health at risk” and “undermining the historic vaccination efforts.”

Also Read What are the differences of these various COVID-19 vaccines?

Prioritizing The Elderly

When there is an unstable supply chain, most experts agree that the priority should be to give the elderly and long-term care residents the two doses on time.

Dr. Isaac Bogoch, an infectious disease physician at Toronto General Hospital, said the focus in Ontario is to put all the resources into vaccinating those who are most vulnerable and at greatest risk of death.

We know that people in long-term care are typically older or have other health problems, (yet) are just less likely to mount the same immune responses as otherwise healthier, younger individuals. So, the goal is really to give those two vaccine doses as per that schedule to those who live in long-term care. I think that’s very reasonable,” he told Global News.

As for the rest of the population, provinces should not purposely delay the second dose beyond the 42-day mark, he added.

“That 42 days is the maximum, it’s not the goal, … and if people can be closer to that day 21 goal, the better,” Bogoch said.

According to recent modelling data from researchers at the University of Toronto, administering most of Canada’s coronavirus vaccines now, as opposed to reserving half of them to be used later as second doses for the first recipients, could prevent a significant amount of new symptomatic COVID-19 infections.

Dr. Anna Banerji, an infectious disease specialist at the University of Toronto, said it is actually better to spread the vaccine to as many people as quickly as possible with a first dose rather than reserving the second shot in case of shortages.

“If the end goal is to save lives and prevent hospitalization and vulnerable populations, then it’s better to get the vaccine out to all the people who are at high risk, like long-term care facilities, first rather than getting two to half the amount of people,” she told Global News.


2. Saba Aziz

Do I Have To Live With Stoma Forever ?

Do I Have To Live With Stoma Forever ?

Live With Stoma Forever ? – In the first blog about stoma before, I mentioned about stoma-forming surgery that could be permanent or temporary.

The formation of an intestinal stoma (usually ileostomy or colostomy) is an integral part of the surgical management of several pathologies of the gastrointestinal tract, in both emergency and elective patients.  A stoma may be created in a temporary or permanent role to reduce morbidity and mortality associated with several conditions of the gastrointestinal including perforation, inflammatory bowel disease, bowel obstruction and elective cancer operations.

Also Read What are the differences of these various COVID-19 vaccines?

A. History of Intestinal Stomas

In the pre-anaesthetic era the formation of intestinal stomas was uncommon. The names of the first few patients whose treatment comprised the forced creation of an intestinal fistula are known. The first among them was George Deppу, who had sustained an abdominal wound during the Battle of  Ramilles on 23 May 1706, after which he had a colostomy formed, which functioned for the remaining 14 years of his life. In 1737, the Queen of Great Britain, Caroline of Brandenburg-Ansbach, the wife of George II, had a spontaneous intestinal stoma (“Royal stoma”) after rupturing the membrane of strangulated umbilical hernia. Because the strangulation led not only to obstruction, but bowel gangrene as well, she died three days later. In 1750, William Cheselden operated on 73-year old Margaret White for strangulated umbilical hernia related to incoercible vomiting  and cut out 55 cm of the intestine, which was fixed at the level of the hernial orifice. Despite the horrible hygiene conditions, she survived and for a long time cared for the peristomal skin with a towel and a rag (Wu 2012, Cromar 1968 Kingsnorth 2006, Cheselden 1750). live with stoma forever

B. Types of Intestinal Stoma

Intestinal stomas can be temporary, diverting stomas designed to rest distal bowel, protect distal anastomoses (e.g. following low anterior resection) or to relieve obstruction.

Permanent stomas are indicated when primary anastomosis is not safe or possible due to the disease process (e.g. gross faecal contamination, poor blood supply or distal bowel resection precluding anastomosis as seen in abdominoperineal resection [APER] when the anus is removed).

Figure I. Different Types of Stoma

Indications for Intestinal Stomas

Table I
Table II

1. Colostomy. How it’s performed

The main surgical techniques are:

  • Open surgery (laparotomy), where the surgeon makes a long incision in the abdomen to access the colon
  • Laparoscopic (or keyhole) surgery, where the surgeon makes several smaller incisions and uses a miniature video camera and special surgical instruments to access the colon

Where possible, keyhole surgery is the preferred choice. This is because research has shown that patients recover quicker and have reduced risk of complications. However, in emergency situations, such as a bowel obstruction, the staff and equipment needed for a keyhole operation may not be available, so an open operation needs to be performed. live with stoma forever

There are 2 main ways a colostomy can be formed, a loop colostomy and an end colostomy.

1.1 Loop Colostomy

To form a loop colostomy, a loop of colon is pulled out through an incision in your abdomen. This section of colon is opened up and stitched to the skin to form an opening called a stoma. The stoma will have 2 openings, but they will be close together and you may not be able to see both.

One of the openings is connected to the functioning part of your bowel. This is where waste products leave your body after the operation. The other opening is connected to the “inactive” part of your bowel, leading to your rectum. This opening only produces small amounts of mucus.

The position of the stoma depends on which section of the colon is diverted, although it’s usually on the left-hand side of your abdomen, below your belt line. If the operation is planned in advance, you’ll meet a specialist and stoma nurse before the operation to discuss possible locations for the stoma. This may not be possible if the operation is performed as an emergency.

The stoma will appear large at first, as the effects of surgery cause it to swell. It usually shrinks during the weeks after surgery, reaching its final size after about 8 weeks. The stoma will be red and moist. It has no nerve endings, so it isn’t painful to touch. It may bleed when touched, but this is entirely normal and no cause for concern. In some cases, a support device (called a rod or bridge) may be used to hold the loop of colon in place while it heals. This will usually be removed after a few days.

A loop colostomy is usually formed temporarily to treat conditions such as diverticulitisCrohn’s disease and bowel cancer.

1.2 End Colostomy

To form an end colostomy, one end of the colon is pulled out through an incision in your abdomen and stitched to the skin to create a stoma.

Like when a loop colostomy is formed, the position of the stoma depends on which section of the colon is diverted. However, it’s usually on the left-hand side of your abdomen, below your belt line.The stoma will have one opening, through which waste products pass. The other end of the colon, which goes down to your rectum, is sealed and left inside your tummy.

End colostomies are often permanent, although temporary end colostomies are sometimes formed as an emergency to treat bowel obstructions, colon injuries or bowel cancer.

Figure 2: (a)End Colostomy and (b)Loop Colostomy

2. Ileostomy, How it’s performed  

2.1 End Ileostomy

An end ileostomy normally involves removing the whole of the colon (large intestine) through a cut in your abdomen. The end of the small intestine (ileum) is brought out of the tummy through a smaller cut and stitched on to the skin to form a stoma. Over time, the stitches dissolve and the stoma heals on to the skin.

After the operation, waste material comes out of the opening in the tummy into a bag that goes over the stoma. This type of ileostomy is often, but not always, permanent.

2.2 Loop Ileostomy

To form a loop ileostomy, a loop of small intestine is pulled out through a cut in your tummy. This section of intestine is then opened up and stitched to the skin to form a stoma. The colon and rectum are left in place. In these cases, the stoma will have 2 openings, although they’ll be close together and you may not be able to see both.

One of the openings is connected to the functioning part of your bowel. This is where waste products leave your body after the operation.

The other opening is connected to the “inactive” part of your bowel that leads down to your rectum.

The loop ileostomy is usually temporary and may be reversed during a second operation at a later date.

Figure 3 completed J-pouch procedure using two loops from the small intestine

2.3  Ileo-anal Pouch

In some cases, it may be possible to have a permanent internal ileo-anal pouch, also known as a J pouch, formed instead of an ileostomy. An ileo-anal pouch is created from the ileum and joined to the anus, so waste material passes out of your body in the normal way.

The pouch stores the waste material until you have a poo. The area around the pouch usually needs to heal before it’s used, so a temporary loop ileostomy may be created above the pouch.

A second, smaller, operation is usually carried out a few months later to close the loop ileostomy.

C. So, I have a chance to not live with my STOMA forever, right?

Due to the explanation above, we can conclude that not all stoma-formed surgery will end up with having stoma forever. There is a chance for stoma patient to have stoma closure/reversal.

The decision to have a reversal operation depends on how much and which part of the bowel has been removed. If very little of the rectum remains, then it is likely that bowel control will be impaired. Your healthcare professional will advise whether stoma reversal is possible, it is estimated that around 35% of ostomates have a temporary stoma.

The main considerations for the stoma reversal are: Journal Reversal of Stoma

  1. The doctors must be happy that you are fit enough for another operation.  n
  2. The bowel that your temporary stoma was created to protect has healed or improved since the first operation.
  3. The anal sphincters which control the flow from your bowels are working, so that loss of control of your bowels (faecal incontinence) will not develop afterwards.

Depending on what operation you have had, the surgeon may need to perform a rectal examination, and possibly arrange some further test before making this decision.

D. What does the surgery involve?

The closure of your stoma is ‘technically’ not as demanding as your previous surgery when the stoma was created. This operation involves making a cut around the stoma, to free it from the tummy wall and stitching the bowel back together to restore continuity, the stitching may be referred to as an anastomosis. The joined bowel is dropped back inside the tummy. This is followed by the stitching of the tummy wall muscles and skin. It is still considered a significant operation. Very occasionally it is necessary to reopen the original laparotomy wound scar to be able to reverse the stoma.

  • Colostomy and Ileostomy Reversal

Basically, both colostomy or Ileostomy have the same procedure during closure/reversal surgery.

If your colostomy/ileostomy is intended to be temporary, further surgery will be needed to reverse it at a later date.

The reversal operation will only be carried out when you’re in good health and fully recovered from the effects of the colostomy formation operation. This will usually be at least 12 weeks or more after the initial surgery.

However, the reversal may need to be delayed for longer if you require further treatment such as chemotherapy, or haven’t recovered from the original operation when the colostomy was formed. There’s no time limit for having the stoma reversed and some people may live with their colostomy for several years before it’s reversed.

In some cases, reversing a colostomy may not be recommended. For example, if the muscles that control your anus (sphincter muscles) were damaged after surgery, reversing the colostomy may cause bowel incontinence.

Reversing a loop colostomy is a relatively straightforward process. An incision is made around the stoma to allow the surgeon to gain access to the inside of your abdomen. The upper section of your colon is reattached to the remaining section of your colon.

Reversing ileostomy A cut is made around the stoma (like colostomy reversal surgery) and the section of small intestine is pulled out of the tummy. The area that had been divided to form the stoma is then stitched back together and placed back inside the abdomen. But the surgeon will need to make a larger incision to locate and reattach the small and large intestines.

It’s also possible to reverse an end colostomy. However, the surgeon needs to make a larger incision to locate and reattach the 2 sections of the colon. Therefore, it takes longer to recover from this type of surgery and there’s a greater risk of complications.

E. What to expect after surgery

You may have a drip in your arm to give you fluids until you are drinking.  Once you are awake you can eat and drink normally, you may find small, light, low fiber meals are better tolerated. Most people are moderately sore at the reversal site afterwards, but this can be managed with pain killers. You may feel distended following the procedure, some patients describe this as a  feeling of being “bruised and bloated” but as the swelling decreases this discomfort will ease.

Possible side effects after stoma closure:

  • Diarrhea – After the reversal it is common to experience liquid bowel motions for the first few days up to a few weeks before it settles down. In a small percentage of patients it can take up to 6 months before the bowel motions become more firm. It is fairly common to pass looser and more frequent stools than you may have been used to previously. Adjusting the food you eat and taking bowel slowing medication can help with this.
  • Frequency and urgency – It is normal to have erratic bowel movements for several weeks after this operation. You may find that you need to go to the toilet more urgently and also more often. This can be more of a problem for those who have had a low join or anastomosis in the bowel and for those who have had pelvic radiotherapy and/ or were already suffering from a weak sphincter muscle. The patients who have weak pelvic floor and anal sphincter muscles may leak gas, liquid or solid stools.  Performing pelvic floor exercises may help to regain continence but need to be practiced at least five times a day and over a few months to be of benefit. When done correctly, these exercises can build up and strengthen the muscles to help you to hold both gas and stool in the back passage. Good hygiene and a light barrier cream may be useful to prevent the skin becoming sore if you are experiencing loose and frequent stools.
Figure 4 Representative abdominal images. (a)before ileostomy reversal, (b)before and (c)after application of NPWT(Negative-Pressure Wound Therapy), and (d)3 days, (e)30 days, and (f)90 days after ileostomy reversal. (Journal: 10.1007 Evaluation of negative‑pressure wound therapy for surgical site infections after ileostomy closure in colorectal cancer patients: a prospective multicenter study)


  2. . History of Medicine 6(2): 111-117
  3. Ileostomy how it’s performed. January 20th  2020
  4. . Ostomy Day: 9 myths about having stoma. January 20th 2020

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