Is asthma a disease of sunlight/vitamin D deficiency?

Yes. Asthma, to a great extent, is caused by sun avoidance and consequent vitamin D deficiency.

Asthma, a devastating respiratory illness, is increasing rapidly in the US. The latest statistics I have show that the overall prevalence of asthma increased 75% from 1980-1994, and asthma rates in children under the age of five increased more than 160%.[1]

There is little doubt that the profound increase in asthma in the last few decades has been caused to a great extent by our societal exodus from sunlight exposure along with the increased use of sunscreen, which can inhibit up to 99% of vitamin D production by the skin.[2]

Drs Litonjua and Weiss, in a medical hypothesis presented in 2007, made a strong case for vitamin D deficiency as a major player in the increase in asthma incidence among both children and adults.[3] They hypothesized the following:

1. “… as populations grow more prosperous, more time is spent indoors, and there is less exposure to sunlight, leading to decreased cutaneous vitamin D production.”
2. “Vitamin D has been linked to immune system and lung development in utero, and our epidemiologic studies show that higher vitamin D intake by pregnant mothers reduces asthma risk by as much as 40% in children 3 to 5 years old.”
3. “Vitamin D deficiency has been associated with obesity, African American race (particularly in urban, inner-city settings), and recent immigrants to westernized countries, thus reflecting the epidemiologic patterns observed in the asthma epidemic.”

Other research demonstrates that vitamin D reduces the production of inflammatory chemicals (chemokines) in the respiratory passages,[4] which would dampen the asthmatic response.

Another study assessed the asthma risk of children whose mothers had the highest vitamin D consumption during pregnancy, and compared them to children whose mother had the lowest levels. The high-vitamin D group showed an impressive reduced risk of asthma of 52-67%.[5] The researchers believe that inadequate vitamin D levels in the fetus leads to improper development of the lungs and immune system.

Still other research, conducted on three-year old children whose mothers were in the highest quartile (fourth) of vitamin D consumption during pregnancy, showed them to have a 61% reduced risk of a “recurrent wheeze,” a symptom of asthma, when compared to those whose mothers were in the lowest quartile.[6] Each 100-IU increase in vitamin D consumption resulted in a 19% risk reduction. That’s about the amount that could be produced in the summer sunlight in one minute, or a good tanning bed in half a minute! How sad that these women have been frightened out of the sunlight, the natural way to produce vast quantities of vitamin D.

[1] Centers for Disease Control. Surveillance for Asthma – United States, 1960-1995, MMWR. 1998; 47 (SS-1).
[2] Matsuoka, L. et al. sunscreens suppress cutaneous vitamin D3 synthesis. Journal Clini Endocrinol Metab 1987; 64:1165-68.
[3] Litonjua AA, Weiss ST. Is vitamin D deficiency to blame for the asthma epidemic? J Allergy Clin Immunol 2007;120:1031–1035.
[4] Banerjee, A. et al. Vitamin D and glucocorticoids differentially modulate chemokine expression in human airway smooth muscle cells. Br J Pharmacol 2008; 155: 84–92.
[5] Devereux, G. et al. Maternal vitamin D intake and early childhood wheezing. Am J Clin Nutr 2007;85:853-59.
[6] Camargo, C. et al. Maternal intake of vitamin D during pregnancy and risk of recurrent wheeze in children at 3 y. Am J Clin Nutr 2007;85:788-95.

Feline Heartworm Disease

Cats are very different from dogs when it comes to heartworm disease. Not only do they differ in their susceptibility to the disease, but also in how the disease affects them and how the disease is diagnosed.

There are significant differences between feline heartworm disease and canine heartworm disease. Cats are more resistant to the disease, and typically when they do become infected have a smaller burden of worms in their bodies. But due to their smaller size, even a few worms can be considered a heavy infection for a cat. Even one worm can cause illness or death in a cat.

Heartworms are caused by a parasite called Dirofilaria immitis. Cats and dogs become infected with this parasite through mosquitoes that can carry this parasite. When a mosquito bites the cat, the parasite enters the bloodstream and grows into an adult worm several centimeters long. These worms tend to accumulate around the vessels of the heart and lungs and cause inflammation of these vessels. In severe cases they can cause a thromboembolism which results in an acute death.

Since heartworm disease in cats happens less often than in dogs, cats with heartworm disease are often misdiagnosed. Cats with heartworms are often wrongly diagnosed as having asthma or allergic bronchitis. Also, many cats can have heartworms and not appear ill.

The true percentage of heartworm positive cats is hard to determine due to diagnostic limitations. In dogs an antigen test is the “gold standard” in diagnosing heartworm disease and it is a very accurate test. Unfortunately in cats these tests are not as accurate. In cats several tests must be used together to arrive at an accurate diagnosis. These tests can include serology, x-rays, and echocardiographs.

Cats that are positive for heartworm disease have many treatment options, but they all have risk associated with them. In mild cases an anti-inflammatory like prednisone may be used. This drug helps support cats by reducing the inflammation of affected vessels. For cats showing severe clinical signs, more extensive treatment and hospitalization are needed. Surgery is also an option to physically remove any worms.

There are many medications on the market to help prevent your cat from getting heartworm disease. Monthly preventatives are an option for cats living in areas where heartworm disease is endemic. Even indoor cats may be at risk if windows are left open. Year-round preventative is increasingly being recommended by more veterinarians. Kittens as young as eight weeks can be started on preventatives.

The most common products used for cats include Interceptor, Heartgard, and Revolution. Interceptor and Heartgard are given orally as chewable medication. Revolution is a topical medication that is applied to the hair over the shoulders. At a minimum the medication should be started within 30 days of heartworm transmission season, and continued until at least 30 days after it ends. In most places this means starting the medication in spring and continuing through the fall.

If you live in an endemic area of heartworm disease, be sure to keep your cat on preventative. Talking to your veterinarian is the best source of advice about the prevalence of heartworm in your area.

[ ] is a complex disease

The November 1 issue of Nature has a special section on autism.  Or better put, on all the things we don’t know about autism, and how that has sobered researchers.  Ten years ago, or even fewer, the focus would have been on the hunt for genes for the disease, but now the recognition has set in, as this section shows, that this is a complex disorder, and genes that explain it aren’t going to be found, brain scans don’t yield simple answers, there is no cure, even if we knew causative genes there would be no cure, and so on.

GWAS have indeed identified hundreds of genes that are associated with autism, but they explain perhaps a percent or two of the cases.  The long-standing hope that this would be another Mendelian trait shows just how much Mendel influenced and in fact sidetracked the understanding of disease, albeit inadvertently.  The essence of a Mendelian trait, be it normal or disease, is that it is due to one (or, perhaps two or three) genes and mainly to two alleles (functionally variant states) at the gene.  This means that if one of the alleles is ‘dominant’ its effects are always manifest in an individual, and one has a 50% chance of inheriting the allele–and hence getting the trait–from a parent who has the allele.  Recessive traits behave similarly–one allele is responsible but only if you inherit two copies of it, one from each parent.  Again, each transmission normally occurs 50% of the time.  We’re oversimplifying, but only a bit, and the gist of the message is as we describe (and we’ve described it before; here, e.g.).

A brief primer on ‘Mendelism’
Mendelian traits segregate with these 50/50 probabilities. Sometimes the chance of having the trait even if you have the allele is less than 100%, so dominance (or what is known, mysteriously, as ‘penetrance’) is ‘incomplete’.  When the trait really is just a single-gene trait we can understand it even with incomplete penetrance.  Even if non-genetic factors cause some instances, which are traditionally known as ‘phenocopies’, we can still make correct inferences, though the ability to predict a newborn’s trait is compromised.

Traits that segregated in Mendel’s pea plants

There are legions of well-known Mendelian diseases, of course, and we’ve had methods for finding genes to explain them for decades.  That has been the job of the professional clinic-associated people known as genetic counselors (because they advise parents of potential risk to their future children).  The problem is that this success is matched by the general fact that Mendelian disorders are usually quite rare in the population.  But our major health concerns today are common, not rare, and they are not Mendelian.  They aggregate in families, so that if a relative is affected your chance of being affected is raised, but they don’t segregate with neatly estimable probabilities, and the reason is that they are due to the effects of many genes, each individually very small, plus complex environmental factors.

Back to autism:
So, it’s complex traits like autism that we’re left with now, and for these our methods are lacking.  But the problem can be described in much the same way for all complex traits.  Take this paragraph from the commentary on the genetics of autism (“Genetics: Searching for answers”), for example:

The large databases of autism gene candidates that are now available make the quest to explain autism more complicated than researchers had hoped. But the complexity of the condition is stimulating the expansion of approaches taken and enticing scientists to look beyond straightforward genetic explanations for autism. “We’ve figured out that explaining autism is not simple,” says Geschwind. “But I have a pretty optimistic view. We’re going to continue to make progress — and a lot of it is because of great collaboration in the field and an influx of new people tackling autism.”

Substitute any complex disease for autism and it could be equally apt; heart disease, diabetes, schizophrenia, asthma, multiple sclerosis, even so-called ‘simple’ disorders like familial cancers or Parkinson’s disease, and the same will eventually be true of rare diseases like the periodic paralyses.  The cases vary substantially, just as there’s variation among people without disease (yet), and this is in part because every genome is unique and everyone is exposed to different intrauterine risk factors at different developmental stages, or during childhood and adulthood.  Science is better at explaining observations that are easily and readily replicable than it is unique events.

Wethinks the geneticist doth protest too much!
The posturing and proclamations of surprise at finding complexity is false on the part of geneticists, or else they have been very unaware of basic biological knowledge that has been around since before they were born. We had every good reason to know, decades ago (and some of us wrote as much back then) that such traits were complex–and why that was so.  The reason for the ‘surprise’ is that it counters the disingenuousness of the proclamations that ‘the’ gene(s) ‘for’ the trait would be found by such means as GWAS. 

The new approaches taken, looking ‘beyond straightforward genetic explanations for’ [whatever trait] now include all the existing omics coming online — microbiome, connectome, metabalome, nutriome, etc — as well as epigenomics, which is the study of alterations to DNA that are not to the gene sequence and may or may not be inherited, may or may not be due to environmental factors such as toxins, and so forth (it’s interesting that this is now bringing epidemiology full circle, from environmental factors to genetics and now back to environmental factors again).  Each of these will surely explain some of the susceptibility to complex disease, but just as surely won’t explain it all, or in everyone.

But hungry scientists know enough to keep coining omics categories.  So now we are seeing what,  consciously or not, amounts to using what is either feigned or culpable surprise to market even more scaled-up, larger, longer-term studies, now to include more kinds of ‘omics, including very costly ‘environomics’ (a word we think we’ve just coined but that is sure to arise soon enough).

Once again, the more we know about all this, the more complex it becomes, not less. Success can eventually come from any direction of course, but we think slowing down the rat-race, calming down and spending more time thinking and less time proclaiming, more musing and less marketing, smaller and more focused rather than all-inclusive approaches would raise the odds.

And, of course, some things may just be irreducibly complicated whether we like it or not.

late-onset sepsis in premature infants of less than or equal to 32 weeks of gest - European Medicines Agency - Rare disease designations - EU/3/10/755

On 27 July 2010, orphan designation (EU/3/10/755) was granted by the European Commission to Schülke & Mayr GmbH, Germany, for octenidine dihydrochloride for the prevention of late-onset sepsis in premature infants of less than or equal to 32 weeks of gestational age.

What is late-onset sepsis?
Late-onset sepsis is a severe bacterial infection of the blood that occurs in newborn babies at least three days after birth. Premature babies born eight weeks or more too early (32 weeks of gestational age or less) have a higher risk of late-onset sepsis than other babies. This is because their immune system, skin and moist body surfaces are not yet fully developed, and because they need invasive procedures such as mechanical ventilation (using a machine to help them to breathe) or administration of medicines or feeding by injection, which can put them at risk of infections in neonatal intensive care units.
Late-onset sepsis is a life-threatening condition that is one of the causes of high mortality in premature babies born at 32 weeks of gestational age or less.

What is the estimated number of patients at risk of developing the condition?
At the time of designation, the number of premature babies born at 32 weeks of gestational age or less was estimated to be approximately 1.5 people in 10,000 in the European Union (EU)*. This is equivalent to a total of around 76,000 babies, and is below the threshold for orphan designation, which is 5 people in 10,000. This is based on the information provided by the sponsor and the knowledge of the Committee for Orphan Medicinal Products (COMP).
*Disclaimer: For the purpose of the designation, the number of patients affected by the condition is estimated and assessed on the basis of data from the European Union (EU 27), Norway, Iceland and Liechtenstein. This represents a population of 506,500,000 (Eurostat 2010).

What methods of prevention are available?
At the time of designation, no satisfactory methods were authorised in the EU for the prevention of late-onset sepsis in these babies. Common infection-control measures such as hand-washing were used to keep the infection rate as low as possible in neonatal intensive care units. In some cases, antibiotics and skin antiseptics were also used to prevent infection.

How is this medicine expected to work?
Octenidine dihydrochloride is an antiseptic that has been available in the EU since 1997 in two medicines, which also contain alcohol, for disinfecting the skin and moist body surfaces in children and adults. Octenidine dihydrochloride works by blocking the growth of bacteria, fungi and other organisms that can cause infection.
This medicine is an aqueous solution of octenidine dihydrochloride. The absence of alcohol is expected to make it suitable for use on the sensitive skin of premature babies.

What is the stage of development of this medicine?
The effects of octenidine dihydrochloride have been evaluated in experimental models.
At the time of submission of the application for orphan designation, no clinical trials with octenidine dihydrochloride in premature babies born at 32 weeks of gestational age or less had been started.
At the time of submission, octenidine dihydrochloride as single agent was not authorised anywhere in the EU for the prevention of late-onset sepsis in premature infants or designated as an orphan medicinal product elsewhere for this condition.
In accordance with Regulation (EC) No141/2000-of 16 December 1999, the COMP adopted a positive opinion on 8 April 2010 recommending the granting of this designation.

Opinions on orphan medicinal product designations are based on the following three criteriathe seriousness of the condition;the existence of alternative methods of diagnosis, prevention or treatment;either the rarity of the condition (affecting not more than 5 in 10,000 people in the EU) or insufficient returns on investment.Designated orphan medicinal products are products that are still under investigation and are considered for orphan designation on the basis of potential activity. An orphan designation is not a marketing authorisation. As a consequence, demonstration of quality, safety and efficacy is necessary before a product can be granted a marketing authorisation.

EU/3/10/755: Public summary of opinion on orphan designation: Octenidine dihydrochloride for the prevention of late-onset sepsis in premature infants of less than or equal to 32 weeks of gestational age
http://www.ema.europa.eu/docs/en_GB/document_library/Orphan_designation/2010/08/WC500095702.pdf

open here please:
European Medicines Agency – Rare disease designations – EU/3/10/755