Stunning anti-ageing breakthrough could see humans live to 150 and regenerate organs by 2020 'for the price of a coffee a day'

 CHARLIE COE FOR DAILY MAIL AUSTRALIA   September 1, 2018

• A new technique could see the aging process in humans reduced by 50 years
• Researchers from Sydney found mice given the pill lived ten per cent longer
• The molecule could also regenerate certain organs by reprogramming their cells
• The drug could be available to the public in five years following human testing

An extraordinary new anti-ageing technique could see humans live to 150 years old and allow them to regrow their organs by 2020.

Harvard Professor David Sinclair and researchers from the University of New South Wales developed the new process, which involves reprogramming cells.

Dr Sinclair said the technique could allow people to regenerate organs, and even allow paralysis sufferers to move again, with human trials due within two years.

The same researchers also found they could increase the lifespan of mice by ten per cent by giving them a vitamin B derivative pill.

An extraordinary new anti-ageing technique could see humans live to 150 years old and allow them to regrow their organs by 2020 (stock image)

They also said the pill led to a reduction in age-related hair loss, according to The Herald Sun. Professor Sinclair said he hoped the pill would be available to the public within five years and cost the same each day as a cup of coffee.

But the professor from the Department of Genetics at Harvard Medical School warned people not to try to reverse the aging process before the science has been published or peer reviewed.

'We do not recommend people go out and take NAD precursors as they have not yet formally tested for safety,' he said. 

Harvard Professor David Sinclair (pictured) and researchers from the University of New South Wales have developed a process, which involves reprogramming cells

The science behind the new technique involves the molecule nicotinamide adenine dinucleotide (NAD), which plays a role in generating energy in the human body.

The chemical is already used as a supplement for treating Parkinson's disease and fighting jet lag. 

Professor Sinclair, who is using his own molecule to reduce the aging process, said his biological age has dropped by 24 years after taking the pill.

He said his father, 79, has been white water rafting and backpacking after starting using the molecule a year-and-a-half ago.

The professor also said his sister-in-law was now fertile again after taking the treatment, despite having started to transition into menopause in her 40s.

Human testing is due to begin in 2020, and Professor Sinclair said he hoped the pill would be available to the public within five years and cost the same each day as a cup of coffee (stock image)

http://www.dailymail.co.uk/news/article-6121913/New-technique-humans-live-150-regrow-organs-price-coffee-day.html

Monthly Programs : Florida

September 1, 2018

Monthly Programs by County

Charlotte County

Parkinson’s Support Group

2nd Tuesdays @1:30pm

Murdock Baptist Church 18375 Cochran Blvd, Port Charlotte

Parkinson’s Support Group

4th Fridays @ 10:00am

Punta Gorda Civic Association 2001 Shreve St, Punta Gorda

************************

Manatee County

Care Partner (Only) Support

2nd Thursdays @ 10:00am

4th Thursdays @ 10:00am

The Sheridan, 11705 Evening Walk Dr, Lakewood Ranch

Care Partner Connection &Parkinson’s Power Hour1st Mondays @ 1:00pmGoodwill Manasota

2705 51st Ave E, Bradenton

Parkinson’s Support Group

3rd Tuesdays @ 10:00am

Freedom Village: The Inn, 6406 21st Ave W (3rd Floor Dining room), Bradenton

Parkinson’s Café

Seasonal October – April

1st Thursdays 10:00am -2:00pm

Caddyshack Sports Bar & Grille 6600 River Club Blvd, Bradenton

Parkinson’s Education Forum

2nd Tuesdays @ 10:00am

Manatee Memorial Hospital Auditorium

206 2nd St East, Bradenton

Parkinson’s Wellness Club

1st Wednesdays @ 10:00am

SMH @ Heritage Harbour, 1040 River Heritage Blvd, Bradenton

Parkinson’s Women’s Group

3rd Fridays @ 1:30pm

Mocha Joe's Cafe

3633 Cortez Rd W, Bradenton

************************

Pasco County

Parkinson’s Café

Seasonal October – April

2nd Thursdays 10:00am -2:00pm

The Family Fitness Center 4900 U.S. 19 North

New Port Richey

************************

Pinellas County

Parkinson’s Café

Seasonal October – April

3rd Thursdays 10am - 2:00pm

Morean Arts Center,

719 Central Ave, St. Petersburg

Dancing Through Parkinson's

Seasonal: Sept. 4th -Nov. 20th & Jan. 8th -March 26th

Tuesdays @ 10:45-12:00pmAzalea Recreation Center, 1600 72nd St. N., St. Petersburg

Parkinson’s Support Group

Seasonal May – September

3rd Thursdays 10am-11:30am

Mirror Lake Library

280 5th St N, St. Petersburg

************************

Sarasota County

Care Partner Connection & Parkinson’s Power Hour2nd Wednesdays @ 10:00amSMH @ Clark Rd,

5880 Rand Blvd, Sarasota

1st Wednesdays @1:30pm

3rd Wednesdays @ 1:30pm 4th Wednesdays @ 1:30pmNCF Office 5600 Peace River Rd, North Port

3rd Thursdays

Complimentary Lunch: 12:00-1pmGroup Meeting: 1:00pm- 2:00pmRSVP @ 941-364-7560, JewishFamily & Children’s Services, 2688 Fruitville Rd., Sarasota.

Creative Connection:Expressive Art & Healing for PD4th Fridays @ 1:00pmHealthSouth Rehab Hospital, 6400 Edgelake Dr, Sarasota

Sarasota (cont’d)

Mindful Movement Yoga for Parkinson’s DiseaseMondays @ 2:45pm- 4:15pm Thursdays @ 1:30pm-3:00pmPineapple Yoga Studio

517 S. Pineapple Ave. Sarasota

Movers & Shakers Group

4th Thursdays @ 3:00pm

Jacaranda Public Library, 4143 Woodmere Park Blvd, Venice

Off-Key Chorale

Seasonal October – April

Tuesdays @ 1:45-3:00pm

SMH@Clark Rd, 5880 Rand Blvd, Sarasota

Parkinson’s Education Forum

3rd Fridays @ 10:00am

St. David’s Episcopal Church 401 S. Broadway, Englewood

Parkinson’s Support Group

2nd Saturdays @ 10:00am

Goodwill Manasota, 5150 N. Tamiami Trail, Sarasota

PD in Motion

Mondays @ 12:30-1:30pm

Soul Studios, 3303 Bahia Vista St, Sarasota

Parkinson’s Wellness Club

2nd Wednesdays @ 1:30pm

SMH 2345 Bobcat Village Center Rd, North Port

3rd Wednesdays @ 10:00am

SMH@Clark Rd, 5880 Rand Blvd, Sarasota

1st Thursdays @ 10:00am

Jacaranda Trace, 3600 William Penn Way, Venice

Parkinson’s Women’s Group

Seasonal October – May

4th Mondays @ 1:30pm

Goodwill Manasota, 5150 N. Tamiami Trail, Sarasota

Voice Aerobics

4th Thursdays @ 11:00am

NCF Office 5600 Peace River Rd, North Port

Monthly Programs by County

For more information on our educational programs and support services visit www.neurochallenge.org or call (941) 926-6413. *updated August, 1, 2018*

Xadago, Cannabinoids, Opioids May Be Best to Manage Parkinson’s Pain, Review Suggests

AUGUST 31, 2018 BY ALICE MELÃO IN NEWS.

Treatment with Xadago (safinamide) or cannabinoids and opioids may the best therapeutic options to effectively manage pain in patients with Parkinson’s disease, researchers suggest.

The study, “Comprehensive Examination of Therapies for Pain in Parkinson’s Disease: A Systematic Review and Meta-Analysis,” was published in the journal Neuroepidemiology.

Parkinson’s disease is known mostly for its motor symptoms such as muscle rigidity and tremors, but other non-motor symptoms are very common. About 68-95% of Parkinson’s patients suffer with pain, which can significantly affect their quality of life and promote both depression and anxiety.

There are several therapeutic strategies available for Parkinson’s disease, however their potential to manage disease-associated pain is not established.

Parkinson’s Clinic of Eastern Toronto researchers reviewed available data from 24 published reports to explore current treatments’ capacities for pain relief. The reports covered the results of 25 randomized clinical trials and a total of 1,744 patients undergoing therapeutic interventions and 1,610 patients undergoing a control intervention.

The mean age of study participants was 66 years and most were male (61% and 60% in treatment or control groups, respectively). Mean disease duration was of 7.9 in the treatment group, and 7.2 years in the control group.

The treatment with the biggest capacity to reduce pain severity was Xadago, followed by cannabinoids and opioids, multidisciplinary team care and COMT inhibitors, such as Comtan (entacapone) and Tasmar (tolcapone).

Electrical and Chinese therapies also had some capacity to reduce pain, although results between studies were very heterogeneous.

Treatment with the investigative pardoprunox (SLV-308) and surgery had only moderate effect on reducing pain severity, while the weakest effects were in dopaminergic agonists and miscellaneous therapies.

Collectively these findings revealed that Xadago “is an important adjunct to the standard parkinsonian medications for alleviating pain” in Parkinson’s, while analgesics in the form of opioids and cannabinoids can “be effective but not nearly to the same extent,” researchers wrote.

In addition, the team believes this study shows that adjusting levodopa levels with Comtan rather than with dopaminergic therapies may provide greater pain relief.

Still, additional trials focusing on pain management, as well as in its underlying mechanisms in Parkinson’s patients, are warranted to “form a consensus on the effectiveness of these therapies.”

https://parkinsonsnewstoday.com/2018/08/31/xadago-cannabinoids-and-opioids-hold-potential-to-manage-pain-in-pd/

Study Reveals Mechanisms Underlying Pain Processing in Parkinson’s Disease

 AUGUST 31, 2018 BY JOSE MARQUES LOPES, PHD 

A novel pain-sensing brain network links pain in Parkinson’s disease to a specific region of the brain, called the subthalamic nucleus, an animal study has found.

The findings illustrate why this specific brain region is a potential target for pain relief in Parkinson’s, as well as in Huntington’s disease, and other neurodegenerative disorders.

The study, “Revealing a novel nociceptive network that links the subthalamic nucleus to pain processing,” was published in the journal eLIFE.

Pain is one of Parkinson’s non-motor symptoms and may manifest as burning, stabbing, aching, itching or tingling sensations. Scientists believe that these symptoms, which are not directly related to the pain caused by the disorder’s motor symptoms, result from dysfunction of the central nervous system.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN), a brain area involved in motor function that is hyperactive in Parkinson’s patients, is an effective technique to ease motor dysfunction. This surgical treatment also has been shown to weaken pain intensity, but the mechanism underlying this benefit remains unclear.

Early studies have indicated that the STN could be part of a network involved in pain perception, but little is known about the type of sensory stimulus activating this brain area.

“We set out to determine whether the [STN] is involved in translating a harmful stimulus such as injury into pain, and whether this information transmission is altered in [Parkinson’s],” Arnaud Pautrat, the study’s lead author, said in a press release.

The research team from France and the U.K. conducted electrophysiology (electrical activity) experiments in rats subjected to a shock to the hind paw. This showed that neurons in the STN could be separated into three groups, depending on whether their electrical activity increased, decreased or was unchanged upon being shocked. Most of the responsive cells changed their activity specifically after pain stimulation and not other types of stimuli.

Then, the team explored if damage to the STN changed these responses. Results showed that rats with lesions in this brain area took much longer to manifest discomfort in comparison to controls.

Subsequent experiments in a rat model of Parkinson’s revealed that neurons in the STN had higher firing rate (greater activity) and exhibited bigger and longer responses to pain than healthy animals. According to researchers, these findings suggest that Parkinson’s-associated pain is caused by impaired pain processing in this brain area.

To understand where pain signals in the STN could come from, the team focused on the superior colliculus and the parabrachial nucleus, two brain areas that relay damage signal originating from the spinal cord.

Blocking the activity or damaging these regions changed the number of STN cells responding to pain, revealing the key role of both regions. Also, researchers found that the parabrachial nucleus and the STN are directly connected.

“We have found evidence that the [STN] is functionally linked to a pain-processing network and that these responses are affected in Parkinsonism,” said Veronique Coizet, PhD, the study’s senior author. Of note, Parkinsonism is a general term for neurological disorders that cause movement problems similar to those of Parkinson’s patients.

Overall, the team believes this network is possibly implicated in the pain relief achieved with DBS in Parkinson’s patients. Coizet noted that more work is necessary to fully characterize the effects of DBS on the STN in animal models.

“The STN-DBS technique can thus be considered in the future as a new target for the treatment of pain in pharmaco-resistant patients suffering from previously described neurodegenerative disease, but also, for example, in chronic pain disease or pharmaco-resistant patients with certain form of migraine,” researchers wrote.

“Further experiments are now needed to fully characterize the effects deep brain stimulationon this brain region in our experimental models, with a view to finding ways to optimize it as a treatment for pain caused by Parkinson’s and other neurological diseases,” Coizet added.

https://parkinsonsnewstoday.com/2018/08/31/study-reveals-mechanisms-underlying-pain-processing-parkinsons-disease/

Liver disease drug could help restore cells damaged by Alzheimer's

 August 31, 2018 by Amy Huxtable, University of Sheffield

PET scan of a human brain with Alzheimer's disease. Credit: public domain

A drug which has been used to treat liver disease for decades could help to restore cells damaged by Alzheimer's, a new study from the University of Sheffield has found.

The pioneering study, funded by Alzheimer's Research UK, discovered the drug ursodeoxycholic acid (UDCA) improves mitochondrial dysfunction – which is known to be a causative factor for both sporadic and familial Alzheimer's disease.

Mitochondria play a pivotal role in both neuronal cell survival and death as they regulate energy metabolism and cell death pathways acting as a cell's battery.

Mitochondrial abnormalities have been identified in many cell types in Alzheimer's disease, with deficits occurring before the development of the classical pathological aggregations. The energy changes have been found in many different cells from people with Alzheimer's. It is thought they are one of the earliest changes to occur in the brain cells, perhaps even before symptoms are reported by people living with the disease.

Dr Heather Mortiboys, Parkinson's UK Senior Research Fellow at the University of Sheffield's Institute of Translational Neuroscience (SITraN), said: "For the first time in actual Alzheimer's patient tissue this study has shown that the drug UDCA acid can boost the performance of the cells' batteries, the mitochondria.

"We also found that the drug, which is already in clinical use for liver disease, acts by changing the shape of the batteries which could tell us more about how other drugs can be beneficial in Alzheimer's.

"Most importantly we found the drug to be active in cells from people with the most common type of the devastating disease – sporadic Alzheimer's – which could mean it has potential for thousands of patients." 

Dr Mortiboys, who led the study, added: "As the drug is already in clinical use for liver disease; this speeds up the potential time it could take to get this drug to the clinic for patients."

The ground-breaking research also found the drug changed the shape of mitochondria by redistributing Dynamin-related protein 1 (Drp1) to the mitochondria in people with Alzheimer's skin cells. Drp1 is a regulator of mitochondrial shape and locates at the mitochondria to initiate fission events. It is thought this could have neuroprotective effects in Alzheimer's disease. This study suggests this pathway could be manipulated by drugs which are then neuroprotective in patients themselves.

The next steps could include studies in patient-derived neurons to check for protective effects or, as others have already shown UDCA to be protective in animal models of Alzheimer's disease, steps could be taken to move UDCA to clinical trials.

Alzheimer's disease is the leading cause of dementia worldwide and is the most common neurodegenerative disorder. It currently affects 850,000 people in the UK, with numbers expected to soar to two million by 2051.

Dr Sara Imarisio, Head of Research at Alzheimer's Research UK, who funded the work, said:"Today, around half a million people in the UK are living with Alzheimer's disease. With no new dementia drugs in over 15 years, it's vital we continue to approach Alzheimer's from as many angles as possible.

"Through innovative research we are building a clearer picture of the complexities of the disease and how it develops in the brain. This work suggests a potential new way to target Alzheimer's but needs further exploration before we can know whether this drug used for a liver condition is safe or effective for people with Alzheimer's disease.

"Alzheimer's Research UK receives no government funding for the research we support, and it is only thanks to the generosity of our supporters that we're able to fund vital projects like this."

Previous laboratory studies conducted by SITraN in 2015 showed UDCA could be an effective treatment in halting the progression of Parkinson's disease. The collaborative study demonstrated the effects of the drug in patients that carry the LRRK2 mutation. The study showed improved mitochondrial function as demonstrated by the increase in oxygen consumption and cellular energy levels.

The new research is published in the Journal of Molecular Biology.

Journal reference: Journal of Molecular Biology

Provided by: University of Sheffield 

https://medicalxpress.com/news/2018-08-liver-disease-drug-cells-alzheimer.html

Parkinson's disease: An endogenous protein might become a candidate for drug development

 August 31, 2018, Ruhr-Universitaet-Bochum

Sebastian Neumann, Rolf Heumann, Dennis Paliga, and Fabian Raudzus. Credit: RUB, Kramer

Researchers have modified the protein Nurr1 so that it can enter cells from the outside. Nurr1 deficiency may be one of the causes of Parkinson's disease. Even though Nurr1 has been discussed as a potential target for the treatment of Parkinson's disease, it is unusable in its normal form, as it cannot penetrate cells. A team from Ruhr-Universität Bochum and the US-American National Institutes of Health (NIH) deployed a bacterial import signal in order to deliver Nurr1 into cells. The researchers also demonstrated that the modified protein may have a positive effect on the survival of dopamine-producing nerve cells. They describe their results in the journal Molecular Neurobiology from 18 August 2018.

For the study, Dennis Paliga, Fabian Raudzus, Dr. Sebastian Neumann, and Professor Rolf Heumann from the work group Molecular Neurobiochemistry collaborated with Professor Stephen Leppla from the NIH.

Bacterial protein building block as import signal

Nurr1 is a transcription factor; this means the protein binds to DNA in the nucleus and regulates which genes get read and translated into proteins. Thereby, it controls many properties in cells that produce the neurotransmitter dopamine and that are affected in Parkinson's disease. Dopamine withdrawal in certain brain regions is responsible for the slowness of movement that is associated with the disease.

Since the Nurr1 protein does not usually have the capability of entering cells and, therefore, cannot take effect in the nucleus, the researchers were searching for ways of furnishing the protein with an import signal. They found what they were looking for in bacteria and attached a fragment of a protein derived from Bacillus anthracis to Nurr1. In the bacterium, that protein ensures that the pathogen can infiltrate animal cells. "The fragment of bacterial protein that we used does not trigger diseases; it merely contains the command to transport something into the cell," explains Rolf Heumann. Once the modified protein has been taken up by the cell, the bacterial protein building block is detached, and the Nurr1 protein can reach its target genes by using the cell's endogenous nuclear import machinery.

Nurr1 has a positive effect on the key enzyme of dopamine synthesis

The researchers measured the effect of functional delivery of Nurr1 by monitoring the production of the enzyme tyrosine hydroxylase. That enzyme is a precursor in dopamine synthesis – a process that is disrupted in Parkinson's patients. Cultured cells that were treated with modified Nurr1 produced more tyrosine hydroxylase than untreated cells. At the same time, they produced less Nur77 protein, which is involved in the regulation of programmed cell death.

Protein protects from the effects of neurotoxin

Moreover, the researchers tested the effect of modified Nurr1 on cultured cells that they treated with the neurotoxin 6-hydroxydopamine. It causes the dopamine-producing cells to die and is thus a model for Parkinson's disease. Nurr1 inhibited the neurotoxin-induced degeneration of cells.

"We hope we can thus pave the way for new Parkinson's therapy," concludes Sebastian Neumann. "Still, our Nurr1 fusion protein can merely kick off the development of a new approach. Many steps still remain to be taken in order to clarify if the modified protein specifically reaches the right cells in the brain and how it could be applied."

More information: Dennis Paliga et al. Lethal Factor Domain-Mediated Delivery of Nurr1 Transcription Factor Enhances Tyrosine Hydroxylase Activity and Protects from Neurotoxin-Induced Degeneration of Dopaminergic Cells, Molecular Neurobiology (2018). DOI: 10.1007/s12035-018-1311-6 

Provided by: Ruhr-Universitaet-Bochum 

https://medicalxpress.com/news/2018-08-parkinson-disease-endogenous-protein-candidate.html

Discovery of long-lived macrophages in the intestine

August 31, 2018, KU Leuven

Macrophages are not just the vacuum cleaners of the immune system. They also support other cells. These long-lived macrophages in the intestines of mice (in green) make contact with the nerve cells of the gastrointestinal tract (in red). The macrophages provide growth factors for the nerve cells. The nerve cells die off without the macrophages. Credit: © TARGID - KU Leuven

Macrophages are specialised immune cells that destroy bacteria and other harmful organisms. Scientists at KU Leuven, Belgium, have come to the surprising conclusion that some macrophages in the intestines of mice can survive for quite some time. Most importantly, these long-lived macrophages are vital for the survival of the nerve cells of the gastrointestinal tract. This sheds new light on neurodegenerative conditions of the intestine, but also of the brain.

In the immune system, macrophages play the role of Pac-Man: They are white blood cells that clean up foreign substances by engulfing them. Apart from this, macrophages themselves provide vital growth factors and support many tissues in the body, allowing them to function and develop properly. As such, these specialised immune cells are soldier and nourisher at the same time. Their proper functioning is immensely important in the intestine, as they have to differentiate between harmful bacteria, harmless bacteria and nutritional components.

Scientists assumed that macrophages in the intestine live for about three weeks at most in both mice and humans before being replaced by new cells. A KU Leuven study now shows that this is not entirely true, explains Professor Guy Boeckxstaens. "We've discovered a small percentage of long-lived macrophages in mice. We marked certain macrophages and found that they still functioned after at least eight months. They can be found in very specific places in the intestine, particularly in close contact with nerve cells and blood vessels."

Additionally, the small group of long-lived macrophages play a very important role in the gastrointestinal tract, adds Ph.D. student Sebastiaan De Schepper. "If the long-lived macrophages don't do their job properly, after only a few days, the mice suffer from digestive problems. This leads to constipation or even the complete degeneration of the nervous system in the stomach and intestine." The discovery that long-lived macrophages do, indeed, exist in the intestine and that they are crucial for the normal functioning of the intestine is therefore immensely important.

These new insights offer promising opportunities for further research, concludes Boeckxstaens: "Next, we want to study the role of long-lived macrophages in human diseases where nerve cells of the intestine are affected, for instance in obese and diabetic patients with abnormal gastrointestinal function. Moreover, the results can also be meaningful for brain research. In the brain, we have microglia, similar long-lived macrophages that play an important role in neurological conditions such as Alzheimer's and Parkinson's disease. Scientists currently believe that nerve cells in these patients die off because microglia do not provide sufficient care. Maybe one day, research of the intestine can offer us a better understanding of these brain conditions."

More information: Sebastiaan De Schepper et al, Self-Maintaining Gut Macrophages Are Essential for Intestinal Homeostasis, Cell (2018).  DOI: 10.1016/j.cell.2018.07.048 

Journal reference: Cell

Provided by: KU Leuven

https://medicalxpress.com/news/2018-08-discovery-long-lived-macrophages-intestine.html

Mediterranean diet shown to prolong seniors' lives

Catharine Paddock PhD   August 31, 2018

A study of older adults by researchers in Italy suggests that the recipe for a longer life is to follow a Mediterranean diet.

Many studies have already hailed the benefits to health and longevity of the Mediterranean diet, but few have focused on older people.

The new research has come from the I.R.C.C.S. Neuromed Mediterranean Neurological Institute in Italy and comprises two parts.

The first is a study that followed 5,200 people aged 65 and older for approximately 8 years.

The second is an analysis that added data from several other studies, bringing the total of older individuals evaluated to 12,000.

In a paper on the findings that now features in the British Journal of Nutrition, the researchers describe how they found that the seniors whose food intake most closely matched a Mediterranean diet lived the longest.

First study author Marialaura Bonaccio, an epidemiologist at I.R.C.C.S. Neuromed, explains that while they knew "that the Mediterranean diet is able to reduce the risk of mortality in the general population," they did not know whether this might also be the case for older people "specifically."

She and her colleagues also observed that there was a "dose-response" relationship between diet and survival in seniors: the closer the diet was to a Mediterranean one, the longer the survival.

The findings support the idea that adopting or continuing with a Mediterranean diet could help older people "maximize their prospects for survival," they conclude.

Assessing the Mediterranean diet

Researchers started to define the Mediterranean diet in the 1960s as they compared eating habits and heart risks of people living in Greece and Southern Italy with those of individuals living in Northern Europe and the United States.

As more and more studies have been done, diverse definitions of what constitutes a Mediterranean diet have arisen. While there are some differences, they generally emphasize the following core components:

• high intake of plant foods such as leafy and other vegetables, nuts, fruits, pulses, whole cereals, and olive oil

• moderate consumption of fish, dairy, meat, and red wine

• low intake of eggs and sweets

For their investigations, Bonaccio and colleagues used a 10-point Mediterranean diet score (MDS) based on one that has been used to study Greek populations.

The MDS assesses intake of different foods and also the ratio of unsaturated to saturated fats in the diet.

An MDS of 0 means minimal adherence to a traditional Mediterranean diet, while a score of 9 means maximum adherence.

The study findings

For the first part of the study, the team analyzed the link between adherence to the Mediterranean diet and survival in 5,200 individuals aged 62 living in the Molise region in central Italy. The people had been recruited for the Moli-sani projectduring 2005–2010.

The purpose of the Moli-sani project was to set up a study population that was separate from those that typically feature in health studies, which tend to focus on Northern Europe and the U.S.

The scientists found that over an 8.1-year median follow-up period, for every one-point increase in MDS, there was an associated reduction in risk of death from: all causes, coronary artery disease, cerebrovascular diseases, and diseases not due to cancer or cardiovascular causes.

In the second part of the study, the scientists searched databases for other similar studies that had examined links between the Mediterranean diet and mortality in older people.

They found six studies that matched their criteria, and they added the data from those to the data they had from the Moli-sani cohort. This gave a large pool of data on 11,738 individuals.

Analysis of the pooled data showed a similar pattern to the earlier results. A one-point rise in MDS was linked to around 5 percent reduction in risk of death from all causes.

Furthermore, an analysis of pooled data from three of the studies revealed an "inverse linear dose-response relationship."

Commenting on their findings, the researchers explain that the foods that appear to offer the most protection in the Mediterranean diet are higher intakes of monounsaturated fats, such as in virgin olive oil, and "moderate consumption of alcohol, preferably during meals."

Bonaccio remarks that while they considered "nutrition as a whole," it was interesting to see the foods that "contribute to the 'driving' effect of the Mediterranean diet."

"Our data confirm what has already been observed in numerous epidemiological and metabolic studies, namely that a moderate consumption of alcoholic beverages, if inserted in a Mediterranean food context, is a protective factor for our health."

Marialaura Bonaccio

https://www.medicalnewstoday.com/articles/322941.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202018-08-31&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29