The use of psychiatric medications has jumped alarmingly  over the last 10 years and no one can explain exactly why.

In the US in 2010, 1 in 5 adults took a psychiatric medication. In women it was higher, 1 in 4.

The most commonly used psychiatric drugs by women are antidepressants, and the women most likely to take them are older woman, aged over 64 years. Approximately 24% of these women are taking an antidepressant, a 40% jump in 10 years. The use of atypical  antipsychotics in these women increased 88%.

Women also have a high anti-anxiolytic consumption, twice as many as men. Interestingly, those women taking the most were aged 45 to 65 years. 11% of all these women took an anti-anxiety medication last year.

The age demographic that saw the greatest overall increase however, were adults aged 20 to 44 years. They tripled their use of ADHD medications, anti-anxiety drugs increased by 30%, and atypical antipsychotics increased by 248%.

The number of children taking these drugs continues to alarm health authorities including the neurological societies. In fact, prescription for these drugs to chldren has doubled from 2001 to 2010. This is alarming for a number of reasons. One is that very little research is done on the effects of these drugs on children. Secondly, it is known that they have significant side-effects including suicide and metabolic abnormalities including a much higher risk to obesity, diabetes and heart disease.

In childhood, many more boys than girls are taking medications for ADHD, but this swaps over in adulthood. The use of these drugs by women is higher than men and has increased by 2.5 times over the last 10 years. Even higher in the 20 to 44-year-old group.

The reasons for these increases are likely to be multiple. One that is being debated is that we are being overdiagnosed and overprescribed these drugs. They have well-known and well-documented severe and sometimes fatal consequences. The medical authorities in fact are attempting to prevent doctors from overprescribing them, much like they are trying to do with antibiotics.

The fact that the first line of care of these patients is often pharmacological drug therapy is unconscionable. Natural solutions are very effective, much safer, and eventually produce healthy people.

Tell your doctor to recommend a natural solution first.

Smokers who stop smoking shortly before surgery (recent quitters) seem to have worse surgical outcomes than early quitters. Therefore, concerns have been expressed about stopping smoking within 8 weeks of surgery. This has generated considerable uncertainty in the media and even in hospitals where smoking cessation advice is an important priority.

Researchers therefore conducted a 9 trial meta-analysis in which they say the concerns are unfounded and that all patients be encouraged to stop smoking. The results from some of the previous studies may simply indicate that recent quitting is less beneficial than early quitting, and not that it is risky.

Looking at the data however, we can see why there may be some confusion. The risk of an overall postoperative complication is unclear (relative risk, 0.78; 95% confidence interval, 0.57-1.07). What this says is that the researchers are 95% certain that the average risk for an adverse outcome is somewhere between 43% lower (0.57) and 7% higher (1.07). This is the confidence interval. It tells us where the average risk may lie. The average, or relative risk, is in the middle of the confidence interval at 0.78 (a 22% reduction). I’m getting the reduction percentages by subtracting from 1.00. For example, 1.00 – 0.78 = a 22% reduction.

It is however, even worse for those studies that focused on pulmonary complications (RR, 1.18; 95% CI, 0.95-1.46). This suggests an average risk increase of 18% (Relative Risk ,1.18), but the confidence interval is large (and spans 1.00) so we can’t say. The 95% interval ranges from 5% reduction (0.95) up to to a 46% increase in risk (1.46).

The researchers conclusions were “the concern that stopping smoking only a few weeks prior to surgery might worsen clinical outcomes is unfounded. There is no evidence to suggest that health professionals should not be advising smokers to quit at any time prior to surgery.”

Which sounds very positive and almost conclusive. What they are actually saying is that nobody knows, but the evidence that it worsens outcomes is not there.

I’ve been a little bit sneaky here. I’ve used this post more to point out how researchers reports findings and make their conclusions rather than to highlight the stopping smoking dilema. My concern with this and many similar papers is that they should just come out and say ‘we’ve still got no idea.’ Because at the end of the day they haven’t, and the pulmonary findings actually look more likely to support the concern than not. We just don’t know.

This is a clear case of absence of evidence, not a finding one way or another. The impression you may get from reading the abstract however, is that we’ve sorted this one out, continue as you were. Larger research trials will get sorted eventually.

When you see the phrase “There is no evidence…” you are being told that they don’t know. I think an appreciation of the findings from that perspective enables us to make better decisions. My final point is that smoking is a massive global health problem and a top priority for all your patients and equivocating around surgical complications must not be used as their excuse to continue.

Reference. Myers K, Hajek P, Hinds C, McRobbie H. Stopping Smoking Shortly Before Surgery and Postoperative Complications: A Systematic Review and Meta-analysis. Arch Intern Med. 2011 Mar 14. [Epub ahead of print]

The recent finding that brain grey and white matter diminish with obesity is taken a little further with new MRI analysis finding that some subcortical brain mass is increased.

Interestingly, they are the subcortical brain structures that are involved in feeding behaviour. The obese people had larger left and right amygdalar volume, and their hippocampus was larger on the left. The greater the BMI, the larger the volume difference tended to be.

One suggestion is that the increased brain volume is associated with greater hedonic food memories, however this cannot be deduced from this research. It could be that those with larger volumes of these brain parts are more susceptible to the influences of a poor lifestyle. It is very interesting that the only areas found to be larger in obese people were those associated with feeding behaviour. Either way, it points clearly to a neurological component to the obesity epidemic and would suggest a reason why dietary programs which rely on prolonged compliance are so ineffective.

The psychological concept of ‘finite will’, where we have a finite capacity to resist temptation, suggests we lose resistance to desires over time and so obese people may lose their will more quickly due to a stronger ‘pull to eat’.

We have to wait for further study to indicate whether the brain volume difference is actually contributing to the obesity or is merely coincident.

Reference. Widya RL, de Roos A, Trompet S, de Craen AJ, Westendorp RG, Smit JW, van Buchem MA, van der Grond J. Increased amygdalar and hippocampal volumes in elderly obese individuals with or at risk of cardiovascular disease. Am J Clin Nutr. 2011 Jun;93(6):1190-1195.

It is now well demonstrated  that cancer surgery can promote the growth and spread of the tumour. There is data emerging however, showing that surgery increases the risk of cancer in people without clinical cancer.

Many of us have undetectable microscopic cancers. They are called occult tumours and are very common in the general population. They are maintained in a dormant state by a healthy immune system and a delicate balance between cell proliferation and cell death. They can remain undetected and dormant for a considerable amount of time, even for a lifetime. Most tumours are thought to arise from microscopic tumours that break out of dormancy. Angiogenesis seems to be a critical factor. Tumours cannot grow beyond 1-2 mm in size without initiating angiogenesis.

Surgery is a severe trauma that creates an abrupt and severe metabolic alarm response. The levels of noradrenalin and adrenalin surge activating β₂-adrenergic receptors which increase vascular endothelial growth factor. This can initiate tumour angiogenesis and is called the angiogenic switch. Animal studies show occult tumour growth inititation with surgery can be blocked with drugs that block the β2-adrenergic receptors. This alone can end tumour dormancy.

The catecholamine surge is also accompanied by high coritsol which can persist for several days. The combination of these impairs cell-mediated immunity at a crucial time and allows the tumour to both break dormancy and also to travel in the blood causing micrometastases. It is an interesting concept that tumours require an abrupt change to break dormancy. It is called the Spike Hypothesis. A search for Tumour Dormancy or the Spike Hypothesis brings up quite a few good articles.

Takeaway: Several implications. One is that we can’t take surgery too lightly. It is associated with many risks however tumour risk is not often considered. Also, other traumas will create the same conditions for initiation. Presurgical care to support immune activity and enable appropriate HPA response may reduce these and other complications.

Reference. Goldstein MR, Mascitelli L. Surgery and cancer promotion: are we trading beauty for cancer? QJM. 2011 Mar 12. [Epub ahead of print]

Others references;

Almog N. Molecular mechanisms underlying tumor dormancy. Cancer Lett. 2010 Aug 28;294(2):139-46

Naumov GN, Akslen LA, Folkman J. Role of angiogenesis in human tumor dormancy: animal models of the angiogenic switch. Cell Cycle. 2006 Aug;5(16):1779-87

Indraccolo S, Favaro E, Amadori A. Dormant tumors awaken by a short-term angiogenic burst: the spike hypothesis. Cell Cycle. 2006 Aug;5(16):1751-5

Bisphosphonates, the new class of drugs that are used orally for osteoporosis and intravenously for bone metastases in cancer ironically cause bone degeneration.

The degeneration is called osteonecrosis and generally affects the jaw. Frankly it is death of bone tissue and seems to be due to the drug reducing the ability of the bone to heal, so any trauma to the jaw, especially after dental work, results in irreparable bone damage and so the bone begins to die.

All of the bisphosphonates have this effect. There is also another drug that does this. It is a nonbisphosphonate that acts on bone remodeling, the monoclonal anti-RANK antibody drug called denosumab.

Using bisphophonates for less than 2 years increases the risk of osteonecrosis by 10 times, and use longer than 2 years increases risk by 40 times. The intravenous use in cancer however raises the risk by 300 times.

The risk is further increased by any oral infection with suppuration, having a  dental extraction, being anaemic, or having radiation for head and neck cancer.

Takeaway. Although the risk for this complication is low, and a hip fracture has a very high risk for death, the consequence of the use of this drug are very difficult to manage. There is also an increased risk to atrial fibrillation with bisphosphonate use. Previous studies have also pointed to atypical fractures occurring due to drug use so the bone tissue being formed while on this drug is abnormal. There are many well documented natural bone building nutrients and strategies available so maintaining bone health needs to be a significant focus for your wellness program for both women and men who you think are at risk to bone fracture.

Reference. Fellows JL, Rindal DB, Barasch A, Gullion CM, Rush W, Pihlstrom DJ, Richman J. ONJ in Two Dental Practice-Based Research Network Regions. J Dent Res. 2011 Feb 11. [Epub ahead of print]

Abstract – http://jdr.sagepub.com/content/early/2011/01/04/0022034510387795.abstract

A mother living within 300m of a freeway while pregnant more than doubles her child’s risk of having autism.

Approximately 11% of the U.S. population lives within 100m of a four-lane highway. So if the poximity to dense traffic proves to be contributory to autism or other neurodevelopmental disorders this would have huge health implications.

Air pollution is particularly heavy within 300m of a freeway and this exposure during pregnancy is almost certain to cause a wide range of negative effects in the foetus. Some freeways in Los Angeles for example carry 300,000 vehicles daily and have extremely high concentrations ultrafine particles. The concentration of these particles are high nearest the freeway and drop to background levels at distances of 300m and greater.

Numerous studies show air pollution to affect children especially prenatally. Diesel exhaust particles have endocrine disrupting activity and trans-placentally affect sexual differentiation and alter cognitive function in mice. Prenatal exposure to ozone in rats alters monoamine content in the cerebellum. Prenatal exposure to benzo(a)pyrene decreases neuronal plasticity and behavioural deficits in mice.

Traffic air pollutants induce inflammation and oxidative stress. Post-mortem brain tissue analysis of children with autism shows increased levels of the pro-inflammatory cytokines TNF-α, IL-6, IL-8, and colony stimulating factor II, as well as two markers of TH-1 immune response IFN-γ and IL-8.

Lipid peroxidation, increased levels of nitric oxide and mitochondrial dysfunction are all associated with autism, which may be related to the formation of reactive oxygen species.

Takeaway: It seems reasonably certain that traffic pollution causes neurological problems. Noise may be a contributor. Air purifiers seem like a prudent investment for the large number of people living near busy roads, especially children and pregnant women.

Reference: Volk HE, et. al. Residential proximity to freeways and autism in the CHARGE study. Environmental Health Perspectives, Ahead of Print.

Full text pdf: http://ehp03.niehs.nih.gov/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1289%2Fehp.1002835&representation=PDF

And it even works when those people taking the placebo know it’s only a placebo!

Ted Kaptchuk, the author of many traditional Chinese medicine texts including The Web That Has No Weaver, is now Associate Professor at the Harvard Medical School studying the placebo effect.

He studied 80 patients with IBS and gave them either a placebo tablet or no medication. All received the same level of interaction with their health care providers. Those people receiving the placebo were told it was a placebo. They also received tablets out of bottle that was labelled ‘Placebo’ and were told that the tablets were made out of inert substance but which had been shown in clinical trials to produce significant improvement in IBS symptoms, which they have.

59% of people, knowing that they were taking an inert substance, noticed symptom improvement compared to 39% of those not taking any tablets. They also felt better more quickly and did so at a rate equivalent to that shown by people taking medical drugs for IBS.

Takeaway: Resistance to placebo use is mainly due to perceived patient deception issues implicating a lack of informed consent. This result however shows that placebos could be used without deception and may still be effective.

Reference: Katpchuk TJ, et. al. Placebos without Deception: A Randomized Controlled Trial in Irritable Bowel Syndrome. PLos One 2010;5(12): e15591

Full text pdf: – http://www.plosone.org/article/fetchObjectAttachment.action;jsessionid=F693F410AA8157C0662BA7AA643E99FE.ambra02?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0015591&representation=PDF

People with higher blood levels of α-carotene have a lower risk of premature death.

We know that trials on β-carotene supplementation showed no, or maybe negative, effects on cancer, cardiovascular disease, or type 2 diabetes. And that these results were a little surprising because of the premise that free radicals damage proteins, fats and of course DNA and therefore inhibiting this would reduce these conditions. α-carotene may have the protective effects we expected β-carotene to have.

α-carotene is chemically similar to β-carotene, but is approximately 10 times more effective in inhibiting proliferation of human neuroblastoma cells, and it also inhibits liver carcinogenesis. This suggests it has effects beyond its antioxidant capacity and therefore has the capacity to prevent pathological change. But it maybe that its just a marker for higher vegetable consumption which has been shown to prevent many conditions and premature death.

The yellow-orange and dark green vegetables, which have a high α-carotene content, are the most protective against lung cancer vs all other vegetables.

People in this study with α-carotene level between 2 to 5 μg/dL had a 27% lower risk for death. Those with levels of 6 to 8 μg/dL had a 34% lower risk for death, and those with levels of 9 μg/dL or higher had a 39% lower risk for death.

This effect was found across several of demographic subgroups, lifestyle habits, and health risk factors indicating that high vegetable consumption is protective for everyone.

The other interesting points from this is that antioxidant defence is just a part of a nutrients beneficial mechanism and that a broad range of metabolic effects is more important. This highlights the importance of diet and herbs in providing a very broad range of metabolically active molecules.

Getting the diet right is fundamental. Fill people up with natural chemicals that are having physiological effects that we don’t even know about yet.

Reference:

http://archinte.ama-assn.org/cgi/content/short/archinternmed.2010.440v1

The US Department of Health Office of Inspector General released a report this week saying that over 13% of all hospitalised patients experience a major adverse event and 1.5% die from them. And a further 13% experience a minor adverse event.

The major adverse events ranged from pulmonary embolisms to wrong-body-part surgery. Minor events include excessive bleeding and prolonged nausea that cause temporary harm.

Of the major and minor adverse events combined, 44% are preventable.

There are also events that occur that are termed “never events” because they should never happen in a hospital, but they do. These events include death or serious disability associated with medication errors, contaminated devices, falls, and other adverse events.

The report recommended that the appropriate agencies broaden their definition of adverse events and work harder to identify them. They also said they should expand the list of adverse events for which the Dept will not pay the bill and hold hospitals accountable for adopting evidence-based practice guidelines.

The bottom line for us, do whatever you can to stay out of hospital. Stay healthy, stay well.

The pdf of the full report is here – http://oig.hhs.gov/oei/reports/oei-06-09-00090.pdf

Smoking cigarettes whilst pregnant increases the likelihood of having a girl.

Public health policy measures to reduce smoking have reduced cigarette exposure during pregnancy. Surpisingly, this has had an influence on the sex of newborns.

A recent decline in the male:female (M:F) sex ratio seems to relate to pregnancy cigarette smoke exposure.

The M:F sex ratio is 1.14 if no parent smokes, meaning that a nonsmoking couple is 14% more likely to have boy. When both parents smoke during the mother’s pregnancy the ratio drops to 0.77, a 23% higher chance of having a girl.

There is also a dose response effect with heavy maternal smokers (>10 cigarettes per day) were more likely to deliver a female baby than light smokers.

Takeaway: This is an unusual finding that indicates toxins are having a broader effect than we realise. Being able to affect the sex of a child shows a potent and disturbing effect. It may be that smoking is reducing the early survival of male foetuses.

Reference: Parental smoking and increased likelihood of female births. Koshy G, Delpisheh A, Brabin L, Attia E, Brabin BJ. Ann Hum Biol. 2010 Jun 14. [Epub ahead of print] http://informahealthcare.com/doi/abs/10.3109/03014461003742803