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« Good clean fun | Main | This charming man »
Tuesday
Apr202010

Health wars: the phantom menace

Years ago Forest published a report entitled Health Wars: The Phantom Menace. It featured many of the health scares reported by the British media in 2001. I am often reminded of it, especially when I see headlines like "Smoking in pregnancy ups risk of cross-eyed baby".

Yesterday the Telegraph reported that "Women who are obese or smoke during pregnancy can cause their sons to have a low sperm count in adulthood ... Experts warned that a mother’s lifestyle could have a 'major impact' on her son’s future sperm. In fact, choices she makes during her lifetime can be even more important than those he makes during his, at least for sperm production, they believe."

Full story HERE.

Writing for The Free Society, Karen McTigue points out that the report is seriously lacking in actual evidence. According to the Telegraph (although this was not reflected in the scare-mongering headline):

The review found there was no evidence to link exposure to individual chemicals to poor sperm production. However, exposure to complex mixtures of environmental chemicals, as might be experienced in real life, may have an impact on the development of testicles and lead to low sperm counts in adulthood. However, more research would need to be done before a link can be fully proven.

More research? Fancy that! Karen adds that:

Saturday’s Daily Mail revealed that Samantha Cameron was spotted drinking a bottle of Mexican lager on Thursday post [leadership] debate ... Current governmental advice states that pregnant women should not drink at all, which, as with most governmental advice, we should happily go ahead and ignore. In other words, babies or no babies, the government and it’s researchers should back right up and let us worry about our own bodies.

Full article HERE.

Reader Comments (20)

Oooh yes! An updated version would be great (and probably ten times the size). I remember getting the first version (think I've still got it somewhere) and it made fascinating, and often highly amusing, reading. And with health scares these days being so outlandish it would be even funner and more poignant. Plus, with the benefit of time having elapsed between the original and now, you could even have a retrospective section looking at how all those early scares have consistently failed to come to fruition. Go on - do it. Pleeeeese!

April 20, 2010 at 9:45 | Unregistered CommenterMisty

I may of posted this before but will do it again, but it is now proven that second hand smoke (SHS) does not cause lung cancer. There are 3 separate scientific reports here which confirm my point.

On our chromosome 11 is the p53 gene, which stops lung cancer cell multiplication. Smoking causes the p53 gene when it replicates to mutate, allowing lung cancer cells to replicate. This mutation does not occur in non smokers, instead their epidermal growth factor receptor (EFGR) protein mutates instead. These conclusions were reported in The Lancet, “Genetic mutations seem to be more common in patients with tobacco-associated lung cancer than in never smokers. Current evidence indicates that the two types of lung cancer are biologically distinct.”

"...whereas the EGFR-gene is mutated in tumours from non-smokers, and not in smokers. Also, age and sex distribution, therapy response and prognosis are shown to differ between the groups. INTERPRETATION: Lung cancer in never-smokers should probably be regarded as a different disease-entity than smoking-induced lung cancer. This could impact prognosis as well as treatment."

"The fact that the mutation spectrum of the p53 tumor suppressor gene in lung tumors of ETS-exposed nonsmokers generally differs from that found in tumors of active smokers lends additional support to the notion that the majority of tumors found in ETS-exposed nonsmokers have nothing to do with tobacco smoke."

Roy Castle did not die from lung cancer contracted from passive smoking playing the trumpet in smoke filled clubs.

http://www.ncbi.nlm.nih.gov/pubmed/18598932?ordinalpos=1&itool=PPMCLayout.PPMCAppController.PPMCArticlePage.PPMCPubmedRA&linkpos=4

http://www.ncbi.nlm.nih.gov/pubmed/19844277

http://www.ncbi.nlm.nih.gov/pubmed/11726024

April 20, 2010 at 10:14 | Unregistered CommenterDave Atherton

The Mail carried this scarmongering story too but added that environment chemicals also had an impact on pregnant women on their male babies sperm count.
If thats the case how come it doesent affect male babies in China who are bred in the midst of chemical, carbon and fog emissions to a choking degree and that China have banned women from having more than one child due to over population.
As long as the spiel keeps churning out the antis scaremongering rules OK!

April 20, 2010 at 10:50 | Unregistered Commenterann

Dave A -

Once again, many thanks for all your sterling efforts in this area.

Are you collating these findings in a single, coherent volume - or have you already done so ?

April 20, 2010 at 11:17 | Unregistered CommenterMartin V

@Martin V

Funnily you should say that, I am up to 10 sides of A4 and not even 1/3rd of the way through. Have the SCOTH minutes and need to read 700 pages of the 2006 US Surgeon General's report.

Then I hope to publish it.

April 20, 2010 at 17:39 | Unregistered CommenterDave Atherton

Simon,
Is the original "Health Wars: The Phantom Menace" still available? Unfortunately I missed it first time round.
I'd love to read an update on it too.

Looking forward to seeing Dave Atherton's document as well.

April 20, 2010 at 19:40 | Unregistered CommenterTonyW

Dave A -

Jolly good !

Do keep us posted..................

April 20, 2010 at 21:45 | Unregistered CommenterMartin V

TonyW, sorry, only one or two file copies remain. We may revive the idea next year.

April 20, 2010 at 22:48 | Unregistered CommenterSimon Clark

@ Dave A.

Dave,
You posted this information regarding the gene P53 before, and, I must admit that I did not fully understand what you were driving at. I hope that Simon does not mind me going through this matter of gene mutations etc on his blog. It will not take long.

The first thing that bothered me about your statement when I first read it some time ago was that it seems to accept that smoking CAUSES lung cancer. “Smoking causes the P53 gene….to mutate, allowing cancer cells to replicate”. This sentence is not in inverted commas in your post, and so I take it that this is your own opinion, or proven scientific fact. But, it may well be that in writing that particular sentence, you are merely saying what the report says. This sentence needs to be clarified. Is it scientific fact that smoking causes the mutation of the P53 gene?

I am further confused by the seeming indiscriminate use of the words ‘non-smoking’ and ‘never-smoking’. As I understand it, these words mean different things in the statistical analyses. And then the phrase ‘passive smoking’ appears. I am not being awkward, I am merely a little confused.

Let me try to understand. Is what I say next correct, as described by the report that you quote?

‘The cells in everyone’s lungs have the potential to become cancerous. There is a gene, the P53 gene, which stops cancerous cells multiplying.

In active, full-on smokers, this gene can mutate and cease to do its job, in which case lung cells which are cancerous can multiply. This process is specific to smokers.

In non-smokers, never-smokers and passive-smokers, this process does not occur. In these cases, when these people get lung cancer, a different process occurs. Something called the EFGR protein mutates, and this allows the lung cells which are cancerous to multiply.

Thus the processes by which smokers and others get lung cancer differ, and thus it seems reasonable to say that tobacco smoke does not ‘cause’ lung cancer in people who are not full-on smokers, because it is not possible for tobacco smoke to cause the mutation in the EFGR protein.’

Is that correct?

Just one more thing directly connected. I read in the column of Dr James LeFanu in the telegraph some time ago that there is something odd about the belief that smoking causes lung cancer, and that is that lung cancers appear on the OUTSIDE of lungs, and not on the inside. I do not know whether that is true or not, but it makes me wonder what the word ‘epidermal’ in the phrase ‘epidermal growth factor receptor’ means. I thought that the word ‘epidermis’ referred to ‘the skin’. Could this be what Dr LeFanu was referring to when he said ‘on the OUTSIDE’ of the lung?

I really am very curious.

April 21, 2010 at 2:34 | Unregistered CommenterJunican

@Junican

@Simon I hope you do not mind taking up some space here for the debate.

Firstly can I start with a correction the p53 gene is on chromosone 17.

For clarity purposes "non smoking" and "never smokers" who have smoked throught their lifetime by drawing the smoke into their lungs. Those that do draw smoke into their lungs are still scientifically classed as non or never smokers if they consumed =/< 100 cigarettes throughout their lives. There is no evidence that cigar and pipe smokers especially who do not inhale run any higher risk of lung cancer, heart disease or mortality.

Yes EGFR mutations are not caused by cigarette smoke. To contract lung cancer the p53 gene has to mutate.

"The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations." (1)

The last sentence "..rather than to selection of pre-existing endogenous mutations," means that the mutation was not by chance or as the result of a natural occuring mutation.

However p53 mutation by itself by smoking does not by itself "guarentee" lung cancer. Hence relatively few smokers contract lung cancer and the peak age of lung cancer mortality is 65-74 after 40-50 years smoking.

What is crucial is the p53's interaction with p21 on chromosone 6. The function of the p21 is the regulation of the cell cycle. Hence the mutation of p53 may, BUT NOT ALWAYS lead to lung cancer.

"The p21 protein also is important in the stress response. p21 is the major transcriptional target of the tumor suppressor gene, p53; despite this, loss-of-function mutations in p21 (unlike p53) do not accumulate in cancer nor do they predispose to cancer incidence."

It was always thought that smoking caused cervical cancer with a raised risk of 250% or an RR of 2.5. We now know it is the sexually transmitted disease Human Papillomavirus (HPV) is the SOLE cause. The correlation is that promiscuous people tend to spoke. Much of this research was knicked from a certain blogger named Frank Davis.

So let's sum up. Inhaling smokers might or might not mutate their p53 gene. Even if it does mutate a healthy p21 gene on cell division will mitigate these effects. Smoking is a cause of lung cancer by setting off a chain of events of mutation of the p53 gene, which inhibits cell division in the p21 gene which allows carcinomas of the lung to develop.

Whatever, Professors West and Jarvis of ASH will not be sending me honoury Doctorates in the post.


1. http://www.ncbi.nlm.nih.gov/pubmed/12379884?ordinalpos=1&itool=PPMCLayout.PPMCAppController.PPMCArticlePage.PPMCPubmedRA&linkpos=4

2. http://en.wikipedia.org/wiki/P21

April 21, 2010 at 8:48 | Unregistered CommenterDave Atherton

Dave A -

Thanks: I can see why the DOH prefers the Science-For-The-Simple-Minded approach to the SHS issue (more correctly, non-issue).

Just try encapsulating THAT information in a snappy soundbite !

As a matter of interest, have any other 'enviromental' factors (eg benzene, sulphur dioxide etc) been positively identified as possible agents in p53 mutation ?

April 21, 2010 at 9:21 | Unregistered CommenterMartin V

@MartinV

Not only can explain it but after your further request for information I may of found a smoking gun.

The p53 gene can mutate for other reasons.

However the mutation in smokers is specifically the guanine to thymine transversion, known as G -> T transversion. This G to T event never happens in non smokers.

If you look at the attached URL written in 2003 from where I obtained this information is from the International Agency for Research on Cancer (IRAC). The IRAC is the World Health Organization's cancer arm and who produced the 1998 Boffetta paper which said passive smoking causes lung cancer.

"As soon as 1994, Curtis Harris at NCI and Monica Hollstein at IARC, had pointed out
that there were special p53 mutations in lung cancers. They found that many mutations
were of a particular kind called “G to T transversion”

"In 1998, Pierre Hainaut and his collaborators at IARC analyzed the mutations in lung
cancers that were at the time in the IARC p53 database. They found that the positions
of damage by benzo(a)pyrene spotted by Pfeifer and his team were frequently the sites
of mutations in lung cancers of smokers but rarely in lung cancers of non-smokers."

The paper then goes on to describe the tobacco industry trying to argue against the p53 G to T Transversion evidence. However most illuminatingly they say:

"However, the whole argument has been blown up by the identification of distinct mutations in the lung cancers of smokers and of non-smokers."

So even in 2003 the WHO/IRAC knew for sure that passive smoking, second hand smoke and/or environmental tobacco smoke did not cause lung cancer possibly evev at the time of the publication of the Boffetta report.

This deserves a wider audience.


http://www-p53.iarc.fr/download/tobacco.pdf

April 21, 2010 at 11:54 | Unregistered CommenterDave Atherton

Dave A -

Brilliant !

If only Dave's Dimwits had HALF your scientific integrity and sense.

But - having just heard Greg (Mr Environment) Clarke burbling on with his Lib/Lab counterparts about 'renewable energy' etc etc - I think I'd probably settle for a QUARTER.

(Message to Mr Clarke: try saying 'Coal-fired power stations.' It doesn't hurt, I promise - and the Dancing Pixies solution can wait).

Good work, Dave.

April 21, 2010 at 13:45 | Unregistered CommenterMartin V

@Simon
Hope you don't mind my continuing the P53 discussion a little.
Dave A,
Fascinating stuff you have there. Hope you don't mind if I sound a slight note of caution.

I noted that the P53 mutations were produced by exposing cells in-vitro (outside the body) to benzo(a)pyrene rather that to tobacco smoke as such .
Apparently small cell lung cancer accounts for around 16% of all lung cancers. Non-small cell lung cancer accounts for 80% of cases.
Which is interesting, considering this evidence from the McTear vs ITL case.

(Professor Idle was an expert witness for ITL)
"[5.542] Under reference to a figure in his report, Professor Idle said that it had been reported that the p53 gene contained mutations in most types of human cancer, ranging from a frequency of between 13% and 14% in prostate carcinoma, up to more than 70% in small cell lung cancer. The frequency in non-small cell lung cancer, which included mainly adenocarcinoma and squamous cell lung cancer, with a frequency of about 40%, placed this group in the middle of the range, so it was no different from other tumours essentially. Professor Idle said that it was noteworthy that, while 40% of non-small cell lung cancer tumours were reported to have had p53 mutations, 60% did not."

(Richard Doll was an expert witness for McTear)
"[5.302] Finally, Sir Richard was asked about benzo[a]pyrene. He agreed that this substance was produced by everything that was burnt and was present in the air that was breathed. As he had previously said, smoking thirty cigarettes a day was not equivalent to exposure to a strong carcinogen. He had also said that whether cigarette smoke acted even as a weak carcinogen was more difficult to determine, though it was necessary to be careful in the use of these terms, because the quantity of a carcinogen was a factor as well as its strength or weakness: 'The poison is in the dose.'"

April 21, 2010 at 19:33 | Unregistered CommenterTonyW

@Tonyw

My brain hurts.

I have read something similar on further research. One thing for sure is the WHO/IARC has a political agenda and scientific objectivity is the bottom of their list.

April 21, 2010 at 20:50 | Unregistered CommenterDave Atherton

Dave A

Sorry to make things even more confusing, but where does this fit in?

I have been studying the plant.


Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis

"We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells.

Studies to determine the optimal NAD concentrations for responding to DNA damage in breast epithelial cells reveal that DNA damage appears to stimulate NAD biosynthesis and that recovery from DNA damage occurs several hours earlier in the presence of higher NAD or in cells undergoing active NAD biosynthesis.

Finally, analyses of normal human skin tissue from individuals diagnosed with actinic keratoses or squamous cell carcinomas show that NAD content of the skin is inversely correlated with the malignant phenotype.

Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis."
http://www.mentorcorp.com/pdfs-global/nia/study/MappingroleofNADmetabolism.pdf


Niacin and Niacinamide In Flue Cured Cigarette Smoke Condensate August 10 1960
http://legacy.library.ucsf.edu/action/document/page?tid=pnx69d00&page=1


"Niacin deficiency in humans, which leads to low NAD status, causes sun sensitivity in skin, indicative of deficiencies in responding to UV damage."

"Niacin deficient keratinocytes are more sensitive to photodamage, as both poly(ADP-ribose) polymerases and Sirtuins are inhibited by the unavailability of their substrate, NAD+, leading to unrepaired DNA damage upon photodamage and a subsequent increase in cell death.
Furthermore, the identification of the nicotinic acid receptor in human skin keratinocytes provides a further link to niacin's role as a potential skin cancer prevention agent and suggests the nicotinic acid receptor as a potential target for skin cancer prevention agents.
The new roles for niacin as a modulator of differentiation and photo-immune suppression and niacin status as a critical resistance factor for UV damaged skin cells are reviewed here."
http://www.ncbi.nlm.nih.gov/pubmed/19149600

"Vitamin B3 is made up of niacin (nicotinic acid) and its amide, niacinamide"

Vitamin lotion may help skin cancer fight

"Researchers at the New South Wales Cancer Institute painted healthy volunteers with a lotion containing vitamin B3 or nicotinamide.
They found those patients treated with the substance suffered no damage to their immunity when exposed to ultra violet light.

In another first, the study found men were twice as likely to suffer immune damage from the sun than women.
Scientists are not exactly sure how vitamin B3 boosts the skin's defences against cancer.

Tests so far have shown it is safe and effective as a topical treatment.
http://www.abc.net.au/news/health/sophie_scott/newsitems/s1366452.htm

April 21, 2010 at 21:02 | Unregistered CommenterRose2

@Rose2

Hi Rose.

If this is a medical question pertaining to yourself please go and see a doctor.

However the role of NAD is the repair of damaged DNA and they appear to discussing the causation, roadmap of skin cancer and how the body repairs itself.

April 21, 2010 at 23:17 | Unregistered CommenterDave Atherton

If I was Simon, I would let this debate run and run, because there are extremely fundamental issues involved. In the same way that the fiasco of the ‘flying ban’ has eventually (even if it has taken only six days) resolved itself into the question of whether or not the distribution of volcanic ash in the atmosphere is sufficiently dense to damage aircraft engines, so the scientific evidence of damage to lungs and hearts etc due to smoking, or passive smoking, must eventually resolve itself in the same way. The difference, of course, is that, in the case of the flying ban, urgent economical considerations concentrated minds. As regards the smoking ban, there are no similar, urgent considerations. So let the debate run as long as people want to debate the issue.

@ Dave A.

Dave, you did not address the point that I raised in my final paragraph, which was: what is the significance of the word ‘epidermal’ in the phrase ‘epidermal growth factor inhibitor’? What has the ‘epidermis’ (the skin) got to do with lung cancer?

I agree that the science of tobacco smoke is critically important, as well as liberties, but if the science is mumbo-jumbo, then there is no way in which the opinions of eminent professors can be overthrown. Only if the science is able to be comprehended by the common man is there any possibility that the science can work to relieve the ban.

April 22, 2010 at 2:29 | Unregistered CommenterJunican

@Jumican

Epidermal is a generic adjective for any outer layer or covering. This could include skin, but also can be applied to the outside of leaves and this context the outside of a cell.

April 22, 2010 at 5:57 | Unregistered CommenterDave Atherton

@ Dave A.

Thanks, Dave. That has answered my question!

I think that I see that this discussion has been about what happens in and around each individual cell rather than whole tumours. The whole matter is beyond me, I am afraid. It is too comlex, and so I will leave it to you!

April 23, 2010 at 0:55 | Unregistered CommenterJunican

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