Tuesday, August 05, 2014

Molecular Psychiatry , (5 August 2014) | doi:10.1038/mp.2014.84

Original Article

Age-related sperm DNA methylation changes are transmitted to offspring and associated with abnormal behavior and dysregulated gene expression
M H Milekic, Y Xin, A O’Donnell, K K Kumar, M Bradley-Moore, D Malaspina, H Moore, D Brunner, Y Ge, J Edwards, S Paul, F G Haghighi and J A Gingrich
Abstract

Advanced paternal age (APA) has been shown to be a significant risk factor in the offspring for neurodevelopmental psychiatric disorders, such as schizophrenia and autism spectrum disorders. During aging, de novo mutations accumulate in the male germline and are frequently transmitted to the offspring with deleterious effects. In addition, DNA methylation during spermatogenesis is an active process, which is susceptible to errors that can be propagated to subsequent generations. Here we test the hypothesis that the integrity of germline DNA methylation is compromised during the aging process. A genome-wide DNA methylation screen comparing sperm from young and old mice revealed a significant loss of methylation in the older mice in regions associated with transcriptional regulation. The offspring of older fathers had reduced exploratory and startle behaviors and exhibited similar brain DNA methylation abnormalities as observed in the paternal sperm. Offspring from old fathers also had transcriptional dysregulation of developmental genes implicated in autism and schizophrenia. Our findings demonstrate that DNA methylation abnormalities arising in the sperm of old fathers are a plausible mechanism to explain some of the risks that APA poses to resulting offspring.

Tuesday, July 22, 2014

[Genetic, environmental, and epigenetic contribution to the susceptibility to autism spectrum disorders].

Rev Neurol. 2013 Dec 16;57(12):556-68.
[Genetic, environmental, and epigenetic contribution to the susceptibility to autism spectrum disorders].
[Article in Spanish]
Author information


Abstractin English, Spanish
INTRODUCTION:
Autism spectrum disorders (ASD) are common and complex neuropsychiatric disorders in which multiple factors may contribute to the phenotype.
AIM:
To review current knowledge about possible risk factors for ASD.
DEVELOPMENT:
Medline, OMIM and Ensembl databases were searched for possible risk factors, disease and gene information.
CONCLUSIONS:
There is genetic heterogeneity and probably different modes of transmission in ASD. In addition, many cases are related with non-inherited de novo mutations or uncommon alleles with a large effect. The general heritability in these disorders may be lower than previously reported. Some fraction of it may be explained by relatively common alleles that tend to have a small effect. To some extent, susceptibility alleles may have a different influence on the phenotype depending on other genetic or non-genetic factors. Non-genetic factors in the perinatal and postnatal period, including epigenetics, the age of the father and possibly the age of grandparents at conception may be relevant for ASD. The mechanisms involved in the etiology of ASD may be related with synaptic development and connectivity, neurotransmission, signaling, neuroplasticity, and gene expression. Different methods have contributed to understand the etiology of ASD. Linkage and association studies are not appropriate for ASD cases with de novo mutations with a strong effect. The observed increase in ASD prevalence may be related not only with more awareness, changing diagnostic criteria, and environmental exposures, but also with epigenetic changes, and an increasing number of de novo mutations.
PMID: 24288105 [PubMed - indexed for MEDLINE]


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Saturday, June 14, 2014

Strong male bias drives germline mutation in chimpanzees.

Science. 2014 Jun 13;344(6189):1272-1275. Epub 2014 Jun 12.
Strong male bias drives germline mutation in chimpanzees.
Author information


Abstract
Germline mutation determines rates of molecular evolution, genetic diversity, and fitness load. In humans, the average point mutation rate is 1.2 × 10-8 per base pair per generation, with every additional year of father's age contributing two mutations across the genome and males contributing three to four times as many mutations as females. To assess whether such patterns are shared with our closest living relatives, we sequenced the genomes of a nine-member pedigree of Western chimpanzees, Pan troglodytes verus. Our results indicate a mutation rate of 1.2 × 10-8 per base pair per generation, but a male contribution seven to eight times that of females and a paternal age effect of three mutations per year of father's age. Thus, mutation rates and patterns differ between closely related species.

Copyright © 2014, American Association for the Advancement of Science.

Thursday, May 22, 2014

Paternal age a determinant of birth success rates with stimulated IUI - Medical News Today

Paternal age a determinant of birth success rates with stimulated IUI - Medical News Today

Wednesday, May 21, 2014

Photographic Proof That Cavities Heal

Photographic Proof That Cavities HealPhotographic Proof That Cavities Heal






29


The compelling article written by Dr. Judene Smith DDS recently about how cavities heal really brought out the conventional dentists in droves! It has been awhile since I had to delete so many nasty, insulting, even threatening comments from a single blog post!
A sad testament indeed to how closed-minded and condescending a large portion of the dental community can be even toward one of its own.
The truth is that cavities can heal and the vehement denial by conventional dentists who react in a defensive manner (as if they have all the answers) does not change this fact one iota.
To drive another nail in the coffin of the notion that cavities must be filled and can’t remineralize and heal on their own, I am presenting a series of photographs sent to me by Rami Nagel, author of the paradigm shattering book Cure Tooth Decay.
The photos are of an 18 month old child from Baton Rouge, Louisiana.  Rikki, the boy’s mother, took these photos as her son’s cavities remineralized over a period of 8 weeks after commencing a dietary program which included supplementing with fermented cod liver oil and high vitamin butter oil.  It is important to note that regular cod liver oil will not produce the same spectacular results you see in these photos.
The sad truth is that when a parent brings in a child with significant tooth decay, toxic, IQ lowering fluoride treatments, drilling/filling or even crowns and root canals are recommended on baby teeth!  These treatments which can be incredibly expensive are not necessary as in a majority of cases, children’s teeth will quickly remineralize with dietary intervention. Adult teeth with cavities will heal in similar fashion as long as they have never been drilled or compromised by dental treatments in the past.
What Did This Child Eat That Caused These Cavities?
Possibly the most shocking thing about this story is that this toddler was not eating a junk food diet when these cavities formed.  He was still breastfeeding and eating an all-organic diet.  His favorite foods consisted of graham crackers and flaxseed bread.  He also was fond of organic granola bars which he ate regularly.
The problem with store bought whole grain products is that they are high in anti-nutrients like phytic acid that block mineral absorption. These foods are not a good choice for regular consumption by growing children.
Rikki’s son also ate fruits and vegetables and organic eggs although his mother avoided butter and milk thinking they were bad for him. After reading Cure Tooth Decay, she realized that butter and milk from grassfed cows are very healing and strengthening for teeth and bones. Grassfed dairy also counteracts some (but not all) of the negative effects of the toxins and anti-nutrients in processed grain products from the store.
Foods That Healed this Child’s Teeth
Rikki implemented 4 major changes to her son’s diet in order to achieve the results you see below.
  1. She cut out grains and sugars. This reduced the mineral depletion from the commercial grains and sugar.
  2. She started giving him Green Pasture’s Royal Blend (a combination product of blended fermented cod liver oil and butter oil) which gave her son the needed fat-soluble vitamins to remineralize his teeth.
  3. Her son now gets raw milk and raw milk cheese regularly along with fermented vegetables like pickles.
  4. Their family now uses butter liberally, and Rikki makes homemade broths and soups from pasture raised chicken.
Unfortunately, the earliest picture is of the teeth after 1 week on the new dietary protocol described in Cure Tooth Decay.  There wasn’t a control picture available of what the cavities looked like before any changes were made. Even still, the visual healing that takes place is compelling and should give every parent hope that cavity problems can be dealt with at home with simple dietary changes in the majority of cases.
Will these dietary interventions be easy? Most definitely not if a conventional diet is being followed. For those already eating a whole foods based diet in their home, the changes are much easier to accomplish. Far and away the most difficult change to implement for cavity prone children especially if they attend school is eliminating the processed grain based foods.
What do you think of these photos?  Do they finally put to bed the repeated denials from conventional dentists that cavities don’t heal and must be filled?
*These photographs were used with Mr. Nagel’s permission (source).







Additional Information

- See more at: http://www.thehealthyhomeeconomist.com/photographic-proof-cavities-heal/?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+TheHealthyHomeEconomist+%28The+Healthy+Home+Economist%29#sthash.uQsKlkt9.dpuf

Turns Out Coconut Oil Has A Major Dark Side

Turns Out Coconut Oil Has A Major Dark Side

Tuesday, May 20, 2014

Millions Fall Prey To This Deadly Breast Cancer Myth




Posted on: Tuesday, May 20th 2014 at 9:15 am
Written By: Sayer Ji, Founder

Millions of asymptomatic women undergo breast screening annually because their doctors tell them to do so. Not only are these women's presumably healthy breasts being exposed to highly carcinogenic x-rays, but thousands have received a diagnosis of 'breast cancer' for entirely benign lesions that when left untreated would have caused no harm to them whatsoever.
New Study: 80% of early-stage breast cancers do not progress to more concerning forms (invasive breast cancer) even after 20 years.
A new study published in the International Journal of Cancer titled, "Is carcinoma in situ a precursor lesion of invasive breast cancer?," is bringing much needed attention to a long standing cancer myth that is harming tens of thousands of women each year: that in situ (non- or slow-growing) breast lesions (carcinoma) inevitably progress to malignant cancers that will cause harm or death if left untreated through conventional methods.  This is simply not true. 
The 25-year prospective follow-up study measured the probability of development of invasive breast cancer (BC) following the diagnosis of carcinomas in situ (CIS) by linking the Canadian National Breast Screening Study (CNBSS) to cancer registries and a national vital statistics database. CIS was classified into ductal (DCIS) and lobular carcinoma in situ (LCIS).
The study found that while the average time from the diagnosis of CIS to invasive BC was 6.3 years (±5.6), and the 20-year cumulative incidence probabilities for DCIS and LCIS were 19.0% (95%CI: 11.2, 26.8) and 21.3% (95%CI: 7.1, 35.4) respectively, at 20-year post CIS diagnosis, more than 80% of them remained free of invasive BC.
Clearly, the notion that DCIS and LCIS always progress to invasive cancer, and therefore must be treated aggressively with the present-day 'standard of care' -- lumpectomy, mastectomy, radiation, and chemotherapy -- is disproved.  In other words, the natural history of in situ lesions like DCIS – commonly misidentified by conventional oncologists as 'cancers' – indicate they progress to invasive breast cancer only 20% of the time, even after 20 years without treatment. 
The study concluded:
"This low probability of developing invasive BC post CIS diagnosis does not support the notion that CIS of the breast is an obligate precursor lesion of invasive BC."
Even 'Invasive Breast Cancer' Is Misunderstood
The misunderstanding about in situ breast lesions extends to so-called 'invasive breast cancer' (BC) as well. Whereas invasive BC is considered by the conventional medical establishment as a lethal disease process that must be cut, burned or poisoned out of the body as soon as it is found, there is great heterogeneity within this biological category, including forms with very low (indolent) and high risk for progression and death, and the whole gamut types between.  Also, several years ago, the journal Lancet Oncology found that some clinically verified "invasive" cancers appear to regress with time if left untreated, further complicating matters:
"Because the cumulative incidence among controls did not reach that of the screened group, we believe that many invasive breast cancers detected by repeated mammography screening do not persist to be detected by screening at the end of 6 years, suggesting that the natural course of many of the screen-detected invasive breast cancers is to spontaneously regress." [emphasis added]
The present inability of the conventional medical system to identify any clear method to determine the difference between a benign, malignant, or possibly regression-prone form of BC, puts the patient at profound risk of overdiagnosis and overtreatment, the consequences of which can be devastating. The lack of individualized treatment and informed choice leads many women to undergo treatment who may have never experienced disease progression had they chosen to employ watchful waiting, or alternative approaches.
The Larger Issue: 'Cancer' Has Been Completely Misunderstood To The Detriment of Millions
A 2013 study published in JAMA titled, "Overdiagnosis and Overtreatment in Cancer: An Opportunity for Improvement,"[1] explains that the word cancer is highly misunderstood and misused.  It has become clear that after 30 years of cancer screening with an emphasis on 'detecting cancer early,' the goals of such campaigns to reduce the rate of late-stage disease and decrease cancer mortality has clearly not been realized. [See video for an in-depth explanation.] This would not happen if the exponential increase of diagnoses and treatment for 'early stage' cancer produced as a result of mammography screening over the past 25 years were actually finding 'cancers,' and not so-called indolent lesions of epithelial origin – i.e. benign lesions that will not progress to malignancy. 
The new study expanded on these implications:
"What has emerged has been an appreciation of the complexity of the pathologic condition called cancer. The word "cancer" often invokes the specter of an inexorably lethal process; however, cancers are heterogeneous and can follow multiple paths, not all of which progress to metastases and death, and include indolent disease that causes no harm during the patient's lifetime. Better biology alone can explain better outcomes."
"Use of the term "cancer" should be reserved for describing lesions with a reasonable likelihood of lethal progression if left untreated. There are 2 opportunities for change. First, premalignant conditions (e.g., ductal carcinoma in situ or high-grade prostatic intraepithelial neoplasia) should not be labeled as cancers or neoplasia, nor should the word "cancer" be in the name. Second, molecular diagnostic tools that identify indolent or low-risk lesions need to be adopted and validated. Another step is to reclassify such cancers as IDLE (indolent lesions of epithelial origin) conditions."

Fundamentally, overdiagnosis results from the fact that screen-detected 'cancers' are 
disproportionately slower growing ones, present with few to no symptoms, and would never progress to cause harm if left undiagnosed and untreated.  The figure below depicts four arrows representing four types of abnormal cell growth: 1) Fast 2) Slow 3) Very Slow 4) Non-Progressive. 

Unless the abnormal cell growth reaches a size at which cancer symptoms occur, it is not justifiable to treat it; nor is it appropriate to call it 'cancer,' as technically it is an indolent or benign lesion. Faster growing cells can contribute to symptoms over a life time, but even then, that does not mean that it will necessarily progress to cause death before natural or other causes take the patients life. In fact, premature treatment can greatly reduce the quality and length of life due to the side effects of chemotherapy, radiation, surgery, and the added stress and psychospiritual trauma of receiving a diagnosis.
The Implications of This Cancer Reclassification To the Healthy and  'Cancer Survivors'
There are two primary implications of this reclassification of 'cancer.' First, those undergoing 'preventive' cancer screening need to be aware of how frequently overdiagnosis occurs (up to 50% within 10 years), especially in breast, lung, prostate and thyroid 'cancers'-- the most prevalent lesions overdiagnosed through routine screening, and indiscriminately treated regardless of differing risk stratifications.  For instance, before the advent of mammography, only 3% of detected breast cancer were identified as DCIS.[2] Today, more than one-third of screen-detected early cancers are DCIS, with the unfortunate result that 33% of those diagnosed with DCIS receiving breast removal (mastectomy), 48% receiving lumpectomy and radiation treatments, 16% receiving lumpectomy, and only 3% electing to do nothing.[3]  The fact that DCIS will do no harm in at least 80% of the time reveals a great burden of iatrogenic harm is being borne by women who are being coerced by an outdated treatment model that is no longer sufficiently evidence-based.
Second, there are now millions of formerly screened, and subsequently treated, patients who had indolent lesions of epithelial origin, such as DCIS, LCIS, or in the case of men, high grade intraepithelial hyperplasia (HGIH) ('prostate cancer'), whose diagnoses were invalid and should never have been treated. For instance, it has been estimated that 1.3 million women were falsely diagnosed with and treated for 'breast cancer' in the past 30 years.  These patients believe they are 'cancer' survivors, when in fact they are surviving the psychospiritual and physical traumas and abuses of their treatments and not their 'disease.' While not knowing the truth may be considered somewhat protective against further trauma associated with no longer identifying with the aggressor – i.e. the conventional medical model – and the potentially devastating realization that they have succumbed to disfigurement and poisoning from unnecessary treatments, along with co-option by cause marketing campaigns – Breast Cancer Awareness Month; Pink Ribbons; Race for the Cure -- encouraging them to act as brand ambassadors for breast cancer associated products and services, and drawing other otherwise healthy women into receiving unnecessary and/or dangerous diagnoses and treatments generated by screening programs. This process I have described in the context of the breast cancer industry 'memeplex,' which I presented on in Washington in 2013 at the Mind-Body Week Conference. You can watch part of my lecture here.
Moving the Paradigm Forward
Over the past few years, a number of studies have been published revealing a paradigm shift in our understanding of cancer. Some of these findings reveal:
For additional research on natural/integrative cancer treatments and the unintended, adverse effects of conventional ones, view the following health guides on Greenmedinfo.com:



[2] Laura Esserman, MD, MBA; and Michael Alvarado, MD  Setting a Research Agenda for Ductal Carcinoma In Situ That Meets the Current Need for Change Ann Intern Med. 2014;160(7):511-512. doi:10.7326/M14-0435


[3] IBID

6 Metabolism Death Foods

by Dr. Josh Axe



There is nothing worse than starting an exercise program, making some good diet changes, but still not seeing the results you want to see.  Has that ever been you?  It can be really frustrating.
The reason this happens is, even though you think you’re consuming a healthy diet, there is often some hidden food in your diet that is ruining your weight loss efforts.
The foods that keep you from losing the last 10 pounds and keep you stuck at a plateau are what I call the metabolism death foods!
The term may sound scary, and it can be.  Your body recognizes these foods as toxins and puts your body into a fight or flight response.
These foods alter the focus of your metabolism and can cause:
  • Weight gain
  • Thyroid dysfunction
  • Fatigue
  • Hormone imbalance
  • Digestive disease
And the craziest thing about these foods is that they are often labeled as “health foods”.
Here are the 6 metabolism death foods you need to switch out of your diet to take your metabolism and fat burning potential to the next level!
6 Metabolism Death Foods

1. Fruit Juice – Contrary to popular belief, fat isn’t the first thing that will make you fat, it’s consuming too much sugar.  Drinking fruit juice and consuming too much sugar will absolutely wreck your metabolism!
Fruit juice including most apple, orange and grape juice is basically chemically laden sugar water! I know something like apple juice sounds healthy, but the process of turning an apple into juice is as follows.
First, they press the apple and remove all of the fiber, then they heat it up through pasteurization at 280 degrees, then it’s dried and turned into a concentrate, then finally, they add in sugar, food coloring and flavorings and that is the apple juice you buy today.
One 8 ounce glass of fruit juice contains 30 grams of sugar where a soda contains 28 grams of sugar!
Also, you should avoid other forms of sugar which can hide under names like: corn syrup, dextrose, fructose, juice concentrate, maltodextrin, raw sugar and brown sugar.
What to do instead:  To replace fruit juice I recommend making homemade lemonade mixing real lemon juice, water and stevia.  Kombucha is another great option as well as herbal tea mixed with raw honey.  Or, drinking coconut water which is nature’s gatorade is another great option!

2. Whole Grains – Whole grains may be the #1 offender when it comes to ruining your metabolism and weight loss efforts.  I know it may seem like “whole grains” like wheat bread are healthy but most are far from helping your metabolism.
Three of the main compounds in grains hurt your metabolism include gluten, starch and phytic acid.  Gluten causes inflammation, starch turns into sugar quickly and phytic acid binds to minerals so you’re not getting most of the minerals and vitamins from whole grains that could have helped your metabolism.
Some of the biggest whole grain offenders include: bread, pasta, cereal, crackers, muffins, desserts, flours, chips and granola bars.
What to do instead: A better option for fat loss is replacing your daily intake of grains with fruits and vegetables or consuming up to 1 piece daily of a sprouted grain bread or sourdough.  Also, the best flour replacement to use instead of wheat flour is coconut flour.  Coconut flour is a dieters best friend because it’s high in fiber which supports rapid fat loss and contains fats your body can burn as fuel.

3. Canola Oil – Using the wrong type of oil can keep you from losing that last 10 pounds and put a halt to any results you might see.  If you use canola oil or other vegetable oils it’s sure to slow down your fat loss efforts and cause you to store unwanted body fat.  Canola oil contains hydrogenated oils which cause inflammation throughout the entire body disrupting your hormones and metabolism.
Also, 90% of canola oil is genetically modified (GMO), which means they are hard wired with pesticides that cause cellular toxicity which destroys your bodies metabolism and overall health.
What to do instead: Replace all vegetables oils with coconut oil and grass-fed butter to boost your metabolism.  I always say, butter is your belly’s best friend.  Grass-fed butter supports metabolism because it is high in CLA and coconut oil supports fat loss because it’s high in MCFA’s.  Consuming these two sources of fat will turn your body into a fat burning furnace!

4. Peanut Butter – Yes, peanut butter is tasty, but it can also kill your gut health.  Peanuts are grown on the soil and stored moist in silos which then cause them to grow a type of fungus called aflatoxins which can effect the health of your gut.
Peanuts are one of the most common allergens today and have been linked to food sensitivities, leaky gut and a slow metabolism.  This aflatoxin in peanuts can compete with probiotics in your gut which we know damages digestive health.
Also, peanuts are very high in omega-6 fatty acids which can cause serious inflammation in the body.  For these many reasons, peanut butter is a metabolism death food!
What to do instead: If you want to start revving up your metabolism then make a switch to almond butter.  Almonds are high in an amino acid L-arginine which increases HGH production in your body.  This is turn causes your body to build lean muscle which sends your metabolism sky high!
Just 1 tbsp spoon of almond butter with celery, in a smoothie or with some apples are great snacks to re-ignite your metabolism.

5. Granola - This “health food” has had a health halo around it for years but it’s secretly been hiding as a wolf in sheep’s clothing that kills your metabolism.
Today’s granola has many issues in that it’s made up of whole grains and sugar.  Now what’s most surprising about granola is that the honey in it is a major cause of weight gain.  A study at Texas A&M University tested honey and found 76% of it contained no pollen whatsoever and it had been high temperature pasteurized so it is no better than corn syrup!
The combination of gluten, phytic acid and processed honey is what makes this treat lethal to your metabolism and diet goals.
What to do instead: A great replacement to store bough granola is to make homemade sprouted granola.  Simply soak almonds, pecans, cashews and chia seeds in water for 8 hours then set them out for a day on a paper towel.  Then mix these ingredients with raw local honey, raisins, coconut flakes, cinnamon and sea salt.  Place them in a dehydrator or oven and you have a great tasting metabolism boosting snack.

6. Artificial Sweeteners – Of all the metabolism death foods, artificial sweeteners including aspartame and sucralose are probably the most deceiving.
Artificial sweeteners tell the lie that you can satisfy your sweet tooth, with no calories, no guilt and a thinner waist line.  However, aspartame is actually linked to 92 adverse health effects.
Aspartame and sucralose (Splenda) can stimulate your appetite and increase cravings for carbohydrates. The calorie “savings” from consuming foods sweetened with aspartame ends up not saving you anything due to the increase in appetite and therefore calorie consumption.
The MESA study evaluated the effect of diet soda consumption on rates of obesity, metabolic syndrome, and diabetes in over 6,000 participants. It was found that the consumption of just one diet soda per day significantly increased the risk for increased waist circumference and weight gain.

What to do instead: Switch out artificial sweeteners for stevia an all natural no calorie sweetener.  Also, raw honey and dates are other great options.

Millions Fall Prey To This Deadly Breast Cancer Myth


Posted on: Tuesday, May 20th 2014 at 9:15 am
Written By: Sayer Ji, Founder

Millions of asymptomatic women undergo breast screening annually because their doctors tell them to do so. Not only are these women's presumably healthy breasts being exposed to highly carcinogenic x-rays, but thousands have received a diagnosis of 'breast cancer' for entirely benign lesions that when left untreated would have caused no harm to them whatsoever.
New Study: 80% of early-stage breast cancers do not progress to more concerning forms (invasive breast cancer) even after 20 years.
A new study published in the International Journal of Cancer titled, "Is carcinoma in situ a precursor lesion of invasive breast cancer?," is bringing much needed attention to a long standing cancer myth that is harming tens of thousands of women each year: that in situ (non- or slow-growing) breast lesions (carcinoma) inevitably progress to malignant cancers that will cause harm or death if left untreated through conventional methods.  This is simply not true. 
The 25-year prospective follow-up study measured the probability of development of invasive breast cancer (BC) following the diagnosis of carcinomas in situ (CIS) by linking the Canadian National Breast Screening Study (CNBSS) to cancer registries and a national vital statistics database. CIS was classified into ductal (DCIS) and lobular carcinoma in situ (LCIS).
The study found that while the average time from the diagnosis of CIS to invasive BC was 6.3 years (±5.6), and the 20-year cumulative incidence probabilities for DCIS and LCIS were 19.0% (95%CI: 11.2, 26.8) and 21.3% (95%CI: 7.1, 35.4) respectively, at 20-year post CIS diagnosis, more than 80% of them remained free of invasive BC.
Clearly, the notion that DCIS and LCIS always progress to invasive cancer, and therefore must be treated aggressively with the present-day 'standard of care' -- lumpectomy, mastectomy, radiation, and chemotherapy -- is disproved.  In other words, the natural history of in situ lesions like DCIS – commonly misidentified by conventional oncologists as 'cancers' – indicate they progress to invasive breast cancer only 20% of the time, even after 20 years without treatment. 
The study concluded:
"This low probability of developing invasive BC post CIS diagnosis does not support the notion that CIS of the breast is an obligate precursor lesion of invasive BC."
Even 'Invasive Breast Cancer' Is Misunderstood
The misunderstanding about in situ breast lesions extends to so-called 'invasive breast cancer' (BC) as well. Whereas invasive BC is considered by the conventional medical establishment as a lethal disease process that must be cut, burned or poisoned out of the body as soon as it is found, there is great heterogeneity within this biological category, including forms with very low (indolent) and high risk for progression and death, and the whole gamut types between.  Also, several years ago, the journal Lancet Oncology found that some clinically verified "invasive" cancers appear to regress with time if left untreated, further complicating matters:
"Because the cumulative incidence among controls did not reach that of the screened group, we believe that many invasive breast cancers detected by repeated mammography screening do not persist to be detected by screening at the end of 6 years, suggesting that the natural course of many of the screen-detected invasive breast cancers is to spontaneously regress." [emphasis added]
The present inability of the conventional medical system to identify any clear method to determine the difference between a benign, malignant, or possibly regression-prone form of BC, puts the patient at profound risk of overdiagnosis and overtreatment, the consequences of which can be devastating. The lack of individualized treatment and informed choice leads many women to undergo treatment who may have never experienced disease progression had they chosen to employ watchful waiting, or alternative approaches.
The Larger Issue: 'Cancer' Has Been Completely Misunderstood To The Detriment of Millions
A 2013 study published in JAMA titled, "Overdiagnosis and Overtreatment in Cancer: An Opportunity for Improvement,"[1] explains that the word cancer is highly misunderstood and misused.  It has become clear that after 30 years of cancer screening with an emphasis on 'detecting cancer early,' the goals of such campaigns to reduce the rate of late-stage disease and decrease cancer mortality has clearly not been realized. [See video for an in-depth explanation.] This would not happen if the exponential increase of diagnoses and treatment for 'early stage' cancer produced as a result of mammography screening over the past 25 years were actually finding 'cancers,' and not so-called indolent lesions of epithelial origin – i.e. benign lesions that will not progress to malignancy. 
The new study expanded on these implications:
"What has emerged has been an appreciation of the complexity of the pathologic condition called cancer. The word "cancer" often invokes the specter of an inexorably lethal process; however, cancers are heterogeneous and can follow multiple paths, not all of which progress to metastases and death, and include indolent disease that causes no harm during the patient's lifetime. Better biology alone can explain better outcomes."

"Use of the term "cancer" should be reserved for describing lesions with a reasonable likelihood of lethal progression if left untreated. There are 2 opportunities for change. First, premalignant conditions (e.g., ductal carcinoma in situ or high-grade prostatic intraepithelial neoplasia) should not be labeled as cancers or neoplasia, nor should the word "cancer" be in the name. Second, molecular diagnostic tools that identify indolent or low-risk lesions need to be adopted and validated. Another step is to reclassify such cancers as IDLE (indolent lesions of epithelial origin) conditions."

older-paternal-age-reduces-iui-live-birth-rates/article/347487/

http://www.renalandurologynews.com/older-paternal-age-reduces-iui-live-birth-rates/article/347487/

Tuesday, May 06, 2014

April 2014, Vol 71, No. 4 > < Previous Article Full content is available to subscribers Subscribe/Learn More Next Article > Original Investigation | April 2014 Paternal Age at Childbearing and Offspring Psychiatric and Academic Morbidity Brian M. D’Onofrio, PhD1; Martin E. Rickert, PhD1; Emma Frans, MSc2; Ralf Kuja-Halkola, MSc2; Catarina Almqvist, MD2,3; Arvid Sjölander, PhD2; Henrik Larsson, PhD2; Paul Lichtenstein, PhD2 [+] Author Affiliations JAMA Psychiatry. 2014;71(4):432-438. doi:10.1001/jamapsychiatry.2013.4525. Text Size: A A A Article Figures Tables References Comments (2) ABSTRACT ABSTRACT | METHODS | RESULTS | DISCUSSION | CONCLUSIONS | ARTICLE INFORMATION | REFERENCES Importance Advancing paternal age is associated with increased genetic mutations during spermatogenesis, which research suggests may cause psychiatric morbidity in the offspring. The effects of advancing paternal age at childbearing on offspring morbidity remain unclear, however, because of inconsistent epidemiologic findings and the inability of previous studies to rigorously rule out confounding factors. Objective To examine the associations between advancing paternal age at childbearing and numerous indexes of offspring morbidity. Design, Setting, and Participants We performed a population-based cohort study of all individuals born in Sweden in 1973-2001 (N = 2 615 081), with subsets of the data used to predict childhood or adolescent morbidity. We estimated the risk of psychiatric and academic morbidity associated with advancing paternal age using several quasi-experimental designs, including the comparison of differentially exposed siblings, cousins, and first-born cousins. Exposure Paternal age at childbearing. Main Outcomes and Measures Psychiatric (autism, attention-deficit/hyperactivity disorder, psychosis, bipolar disorder, suicide attempt, and substance use problem) and academic (failing grades and low educational attainment) morbidity. Results In the study population, advancing paternal age was associated with increased risk of some psychiatric disorders (eg, autism, psychosis, and bipolar disorders) but decreased risk of the other indexes of morbidity. In contrast, the sibling-comparison analyses indicated that advancing paternal age had a dose-response relationship with every index of morbidity, with the magnitude of the associations being as large or larger than the estimates in the entire population. Compared with offspring born to fathers 20 to 24 years old, offspring of fathers 45 years and older were at heightened risk of autism (hazard ratio [HR] = 3.45; 95% CI, 1.62-7.33), attention-deficit/hyperactivity disorder (HR = 13.13; 95% CI, 6.85-25.16), psychosis (HR = 2.07; 95% CI, 1.35-3.20), bipolar disorder (HR = 24.70; 95% CI, 12.12-50.31), suicide attempts (HR = 2.72; 95% CI, 2.08-3.56), substance use problems (HR = 2.44; 95% CI, 1.98-2.99), failing a grade (odds ratio [OR] = 1.59; 95% CI, 1.37-1.85), and low educational attainment (OR = 1.70; 95% CI, 1.50-1.93) in within-sibling comparisons. Additional analyses using several quasi-experimental designs obtained commensurate results, further strengthening the internal and external validity of the findings. Conclusions and Relevance Advancing paternal age is associated with increased risk of psychiatric and academic morbidity, with the magnitude of the risks being as large or larger than previous estimates. These findings are consistent with the hypothesis that new genetic mutations that occur during spermatogenesis are causally related to offspring morbidity.



Original Investigation | April 2014

Paternal Age at Childbearing and Offspring Psychiatric and Academic Morbidity
Brian M. D’Onofrio, PhD1; Martin E. Rickert, PhD1; Emma Frans, MSc2; Ralf Kuja-Halkola, MSc2; Catarina Almqvist, MD2,3; Arvid Sjölander, PhD2; Henrik Larsson, PhD2; Paul Lichtenstein, PhD2
[+] Author Affiliations
JAMA Psychiatry. 2014;71(4):432-438. doi:10.1001/jamapsychiatry.2013.4525.
Text Size: A A A

Article

Figures
Tables

References

Comments (2)



Abstract
ABSTRACT | METHODS | RESULTS | DISCUSSION | CONCLUSIONS | ARTICLE INFORMATION | REFERENCES

Importance  Advancing paternal age is associated with increased genetic mutations during spermatogenesis, which research suggests may cause psychiatric morbidity in the offspring. The effects of advancing paternal age at childbearing on offspring morbidity remain unclear, however, because of inconsistent epidemiologic findings and the inability of previous studies to rigorously rule out confounding factors.
Objective  To examine the associations between advancing paternal age at childbearing and numerous indexes of offspring morbidity.
Design, Setting, and Participants  We performed a population-based cohort study of all individuals born in Sweden in 1973-2001 (N = 2 615 081), with subsets of the data used to predict childhood or adolescent morbidity. We estimated the risk of psychiatric and academic morbidity associated with advancing paternal age using several quasi-experimental designs, including the comparison of differentially exposed siblings, cousins, and first-born cousins.
Exposure  Paternal age at childbearing.
Main Outcomes and Measures  Psychiatric (autism, attention-deficit/hyperactivity disorder, psychosis, bipolar disorder, suicide attempt, and substance use problem) and academic (failing grades and low educational attainment) morbidity.
Results  In the study population, advancing paternal age was associated with increased risk of some psychiatric disorders (eg, autism, psychosis, and bipolar disorders) but decreased risk of the other indexes of morbidity. In contrast, the sibling-comparison analyses indicated that advancing paternal age had a dose-response relationship with every index of morbidity, with the magnitude of the associations being as large or larger than the estimates in the entire population. Compared with offspring born to fathers 20 to 24 years old, offspring of fathers 45 years and older were at heightened risk of autism (hazard ratio [HR] = 3.45; 95% CI, 1.62-7.33), attention-deficit/hyperactivity disorder (HR = 13.13; 95% CI, 6.85-25.16), psychosis (HR = 2.07; 95% CI, 1.35-3.20), bipolar disorder (HR = 24.70; 95% CI, 12.12-50.31), suicide attempts (HR = 2.72; 95% CI, 2.08-3.56), substance use problems (HR = 2.44; 95% CI, 1.98-2.99), failing a grade (odds ratio [OR] = 1.59; 95% CI, 1.37-1.85), and low educational attainment (OR = 1.70; 95% CI, 1.50-1.93) in within-sibling comparisons. Additional analyses using several quasi-experimental designs obtained commensurate results, further strengthening the internal and external validity of the findings.

Conclusions and Relevance  Advancing paternal age is associated with increased risk of psychiatric and academic morbidity, with the magnitude of the risks being as large or larger than previous estimates. These findings are consistent with the hypothesis that new genetic mutations that occur during spermatogenesis are causally related to offspring morbidity.