Two Exciting Alzheimer’s Advances: A Novel Early Detection Test Using Peanut Butter, and a Study Evaluating Coconut Oil

Story at-a-glance

  • At present, an estimated 5.4 million Americans have Alzheimer’s disease. By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans
  • The ability to smell is associated with the first cranial nerve and is often one of the first senses to be adversely affected by cognitive decline.
  • In patients with Alzheimer’s, the ability to smell peanut butter through the left nostril was found to be significantly impaired
  • Patients diagnosed with mild to moderate Alzheimer’s have been enrolled in a clinical study—the first of its kind—to evaluate the effects of coconut oil versus placebo. Results are expected in about a year
  • Previous investigation suggests that ketone bodies, an alternative fuel for your brain that your body makes when digesting coconut oil, might offer profound healing benefits in the fight against Alzheimer’s disease

At present, some 5.4 million Americans have Alzheimer’s disease, according to the Alzheimer’s Association’s 2011 Alzheimer’s Disease Facts and Figures.1

By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans, rivaling the current prevalence of obesity and diabetes.

Since treatments are few and rarely effective, early diagnosis and prevention become all the more important.

Interestingly, simple tools like a tablespoon of peanut butter and a ruler could potentially be used to confirm a diagnosis of the disease in its early stages. As reported by Medical News Today:2

“Jennifer Stamps, a graduate student in the University of Florida (UF) McKnight Brain Institute Center for Smell and Taste, and her colleagues reported the findings of a small pilot study in the Journal of the Neurological Sciences.3

Stamps came up with the idea of using peanut butter to test for smell sensitivity while she was working with Dr. Kenneth Heilman, one of the world’s best known behavioral neurologists, from the UF College of Medicine’s department of neurology.

…The ability to smell is associated with the first cranial nerve and is often one of the first things to be affected in cognitive decline… She thought of peanut butter because, she said, it is a ‘pure odorant’ that is only detected by the olfactory nerve and is easy to access.”

The pilot study tested the ability to smell of 24 patients diagnosed with mild cognitive impairment. To perform the test, the patient was asked to close their eyes and mouth, and hold one nostril closed while breathing normally through the other.

Using a ruler, the clinician measured the distance between the open nostril and the peanut butter, marking the distance at which the patient was able to detect the distinct odor. After a 90 second delay, the procedure was repeated with the other nostril.

They discovered that those diagnosed with early stage Alzheimer’s (which was done through other clinical testing) experienced a significant difference in their ability to detect the odor between the two nostrils. According to the featured report:

“[T]he left nostril was impaired and did not detect the smell until it was an average of 10 cm closer to the nose than the right nostril had made the detection in patients with Alzheimer’s disease.

This was not the case in patients with other kinds of dementia; instead, these patients had either no differences in odor detection between nostrils or the right nostril was worse at detecting odor than the left one.”

Of course, it’s too early to tell whether this test might be reliable enough to become widely used. More research needs to be done. But according to Stamps, the test can be used to confirm a diagnosis. The team is planning to study patients with mild cognitive impairment next, to assess whether it might help predict a future diagnosis of Alzheimer’s.

Benefits of Coconut Oil Make Headlines Again

In related news, Florida researchers are also looking into whether coconut oil might be of benefit against Alzheimer’s. Three years ago, I published Dr. Mary Newport’s theory that ketone bodies, an alternative fuel for your brain that your body makes when digesting coconut oil, might offer profound benefits in the fight against Alzheimer’s disease.

At the time I said that, should her theory turn out to be accurate, it could be one of the greatest natural health discoveries in a long time. Now, Dr. Newport’s research is being used to launch one of the first clinical trials of its kind to test her theory. The research is being done at the USF Health Byrd Alzheimer’s Institute.

Sixty-five patients diagnosed with mild to moderate Alzheimer’s have been enrolled to evaluate the effects of coconut oil on the disease, compared to a placebo. Dr. Newport hopes to have the results within a year.

This issue strikes close to home for Dr. Newport, whose husband has been battling the disease for years. As reported by CTV News:4

“While there is currently no clinical data showing the benefits of coconut oil on the prevention and treatment of dementia, Newport — whose husband Steve was diagnosed with Alzheimer’s at age 51 — said she began to see improvements after starting him on four teaspoons of coconut oil per day.

‘Before the coconut oil, he could not tie his shoes. His weird slow gait… That improved. He walked normally and he was able to start running again.

He was able to start reading again, his conversation improved dramatically and then over several months we saw improvements in his memory,’ Newport said. Prior to starting him on coconut oil, Newport said none of the existing medications were working.”

Coconut Oil Appears to Be an Ideal Brain Food

There are only two types of fuel your body can convert into energy: carbs/sugar, or fat. Again, ketones are what your body produces when it converts fat (as opposed to glucose) into energy. And a primary source of ketone bodies are the medium-chain triglycerides (MCT) found in coconut oil. In fact, coconut oil contains about 66 percent MCTs.

Medium-chain triglycerides (MCT) are fats that are not processed by your body in the same manner as long-chain triglycerides. Normally, a fat taken into your body must be mixed with bile released from your gallbladder before it can be broken down in your digestive system.

But medium-chain triglycerides go directly to your liver, which naturally converts the oil into ketones, bypassing the bile entirely. Your liver then immediately releases the ketones into your bloodstream where they are transported to your brain to be readily used as fuel.

While your brain is quite happy running on glucose, there’s evidence suggesting that ketone bodies may actually help restore and renewneurons and nerve function in your brain, even after damage has set in. Interestingly, the mechanism of this MCT-ketone metabolism appears to be that your body treats MCTs as a carbohydrate and not a fat.  This allows the ketone energy to hit your bloodstream without the normal insulin spike associated with carbohydrates entering your bloodstream. So in effect, coconut oil is a fat that acts like a carbohydrate when it comes to brain fuel.

How Much Coconut Oil Might You Need?

Therapeutic levels of MCTs have been studied at 20 grams per day. According to Dr. Newport’s calculations,5 just over two tablespoons of coconut oil (about 35 ml or seven level teaspoons) would supply you with the equivalent of 20 grams of MCT, which is indicated as either a preventative measure against degenerative neurological diseases, or as a treatment for an already established case.

While more research certainly needs to be done in this area as well, I see no reason not to incorporate coconut oil in your diet, or the diet of a loved one who is exhibiting symptoms of brain degeneration. Coconut oil has so many profound health benefits; it’s not going to do any harm.

It’s worth noting that people tolerate coconut oil differently, and you may have to start slowly and build up to these therapeutic levels. My recommendation is to start with one teaspoon, taken with food in the mornings. Gradually add more coconut oil every few days until you are able to tolerate about four tablespoons. It’s best to take it with food, to avoid upsetting your stomach.

Low-Fat Craze Has Likely Contributed to Dramatic Rise in Alzheimer’s

A number of seriously flawed nutritional guidelines have contributed to more than a few health problems in the US, and the low-fat craze (aimed at preventing heart disease) is toward the top of that list. Not only does avoiding healthful fat promote heart disease, it also promotes brain diseases like Alzheimer’s.

According to neurologist Dr. David Perlmutter, fat avoidance and carbohydrate overconsumption are at the heart of the Alzheimer’s epidemic—which is an entirely preventable disease, driven by lifestyle factors such as diet. Dr. Perlmutter’s book, Grain Brain, provides a powerful argument for eliminating grains from your diet to protect your brain health. Another major factor is the development and increased consumption of genetically engineered (GE) grains, which are now pervasive in most processed foods sold in the US. Unfortunately, despite dire need, there’s little money available for research into treatments using regular food items. As Amanda Smith, Medical Director at University of South Florida (USF) Health Byrd Alzheimer’s Institute told CTV News:

“The pharmaceutical industry is in this — of course to make money for their companies, and of course they want to help people theoretically — but at the end of the day it is about dollars and cents, and so money gets invested in things that are new or patentable rather than things that are sitting on the shelf already.”

Intermittent Fasting Can Also Increase Ketone Production

There are two additional ways to increase ketone production: restricting carbohydrates, and intermittent fasting. Personally, I believe all three of these strategies are best applied together, as you need to replace the lost carbs with high quality fat (and coconut oil certainly fits that bill), and intermittent fasting will help your body shift to burning fat as its primary fuel. It takes about six to eight hours for your body to metabolize your glycogen stores, after which you start to shift to burning stored fat, and hence producing ketone bodies.

Contrary to more stringent and challenging fasts, intermittent fasting simply involves timing your meals to allow your body to enter the fat-burning “window.” To be effective, the length of your fast must be at least 16 hours. For example, this would mean eating only between the hours of 11am until 7pm, or noon until 8pm. You can restrict it even further — down to six, four, or even two hours if you want, but you can still reap many of the health benefits associated with intermittent fasting by limiting your eating to an eight-hour window each day.

I recommend easing yourself into this type of eating schedule. Start by not eating anything for three hours prior to bed, and then gradually extend the time before you eat breakfast each day to the point that you have skipped breakfast and have your first meal at lunch. This typically takes a few weeks to a few months. Also, this is not something that needs to be done continuously once your body has shifted to fat burning mode. However, your desire to eat will be dramatically reduced so you won’t feel the need to eat like you did before shifting your body’s primary fuel burning preference.

Tips for Maintaining Healthy Brain Function and Avoiding Alzheimer’s Disease

Knowing that Alzheimer’s is a preventable disease, predicated on your lifestyle choices, puts the power into your hands.  Diet is paramount, and the beauty of following my optimized nutrition plan is that it helps prevent and treat virtually ALL chronic degenerative diseases, including Alzheimer’s disease.

People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’s entirely possible to prevent the damage from occurring in the first place… and one of the best ways to do this is by leading a healthy lifestyle. The following guidelines will help you protect your brain health well into old age:

Avoid sugar and refinedfructose. Ideally, you’ll want to keep your sugar levels to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you have insulin resistance or any related disorders.

Avoid gluten (primarily wheat). Research shows that your blood-brain barrier, the barrier that keeps things out of your brain where they don’t belong, is negatively affected by gluten. Gluten also makes your gut more permeable, which allows proteins to get into your bloodstream, where they don’t belong. That then sensitizes your immune system and promotes inflammation and autoimmunity, both of which play a role in the development of Alzheimer’s.

Optimize your gut flora by regularly eating fermented foods or taking a high-potency and high quality probiotic supplement.

Increase consumption of all healthful fats, including animal-based omega-3. Beneficial health-promoting fats that your brain needs for optimal function include organic butter from raw milk, clarified butter called organic grass-fed raw butter, olives, organic virgin olive oil and coconut oil, nuts like pecans and macadamia, free-range eggs, wild Alaskan salmon, and avocado.

Contrary to popular belief, the ideal fuel for your brain is not glucose but ketones. Ketones are what your body produces when it converts fat (as opposed to glucose) into energy. The medium-chain triglycerides (MCT) found in coconut oil are GREAT source of ketone bodies, because coconut oil is about 66 percent MCTs. In fact, ketones appear to be the preferred source of brain food in patients affected by diabetes or Alzheimer’s.

Also make sure you’re getting enough animal-based omega-3 fats, such as krill oil. (I recommend avoiding most fish because, although fish is naturally high in omega-3, most fish are now severely contaminated with mercury.) High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder.

Reduce your overall calorie consumption, and/or intermittently fast. As mentioned above, ketones are mobilized when you replace carbs with coconut oil and other sources of healthy fats. A one-day fast can help your body to “reset” itself, and start to burn fat instead of sugar.

As part of a healthy lifestyle, I prefer an intermittent fasting schedule that simply calls for limiting your eating to a narrower window of time each day. By restricting your eating to a 6-8 hour window, you effectively fast 16-18 hours each day. To learn more, please see this previous article.

Improve your magnesium levels. There is some exciting preliminary research strongly suggesting a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately, most magnesium supplements do not pass the blood brain levels, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition and may be superior to other forms.

Optimize your vitamin D levels with safe sun exposure. Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health.

Vitamin D may also exert some of its beneficial effects on Alzheimer’s through its anti-inflammatory and immune-boosting properties. Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation that is also associated with Alzheimer’s.

Keep your fasting insulin levels below 3. This is indirectly related to fructose, as it will clearly lead to insulin resistance. However, other sugars (sucrose is 50 percent fructose by weight), grains and lack of exercise are also important factors. Lowering insulin will also help lower leptin levels which is another factor for Alzheimer’s.

Eat a nutritious diet, rich in folate, such as the one described in my nutrition plan. Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day.

Avoid and eliminate mercury from your body. Dental amalgam fillings, which are 50 percent mercury by weight, are one of the major sources of heavy metal toxicity, however you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.

Avoid aluminum, such as antiperspirants, non-stick cookware, vaccine adjuvants, etc.

Exercise regularly. It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,6 thus, slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has also shown that people with Alzheimer’s have less PGC-1alpha in their brains7 and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s. I would strongly recommend reviewing the Peak Fitness Technique for my specific recommendations.

Avoid flu vaccinations as most contain mercury, a well-known neurotoxic and immunotoxic agent.

Eat blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases. Like any fruit though, avoid excesses here.

Challenge your mind daily. Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.

Avoid anticholinergics and statin drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

Other Natural Treatments for Your Anti-Alzheimer’s Arsenal

Finally, there are a few other nutritional recommendations worth noting for their specific benefits in preventing and treating dementia. So, although your fundamental strategy for preventing dementia should involve a comprehensive lifestyle approach, you may want to consider adding a few of these natural dietary agents to your anti-Alzheimer’s arsenal. These four natural foods/supplements have good science behind them, in terms of preventing age-related cognitive changes:

1.Astaxanthin is a natural pigment with unique properties and many clinical benefits, including some of the most potent antioxidant activity currently known. As a fat-soluble nutrient, astaxanthin readily crosses your blood-brain barrier. One study8found it may help prevent neurodegeneration associated with oxidative stress, as well as make a potent natural “brain food.”

The molecules of astaxanthin neutralize free radicals and other oxidants without being destroyed or becoming pro-oxidants themselves in the process. It’s is a unique molecule whose shape allows it to precisely fit into a cell membrane and span its entire width. In this position, astaxanthin can intercept potentially damaging molecules before they can damage your cells.

You can get some astaxanthin by taking krill oil, which is a fantastic omega-3 fat supplement. But you can boost your astaxanthin even MORE by adding a pure astaxanthin supplement to your nutritional regimen. For optimal absorption, make sure to take krill oil and/or astaxanthin with a fat-containing meal, since both are fat-soluble.

2.Ginkgo biloba: Many scientific studies have found that Ginkgo biloba has positive effects for dementia. Ginkgo, which is derived from a tree native to Asia, has long been used medicinally in China and other countries. A 1997 study from JAMA showed clear evidence that Ginkgo improves cognitive performance and social functioning for those suffering from dementia. Research since then has been equally promising. One study in 2006 found Ginkgo as effective as the dementia drug Aricept (donepezil) for treating mild to moderate Alzheimer’s type dementia. A 2010 meta-analysis found Ginkgo biloba to be effective for a variety of types of dementia.

3.Alpha lipoic acid (ALA): ALA can stabilize cognitive functions among Alzheimer’s patients and may slow the progression of the disease.

4.Vitamin B12: A small Finnish study published in the journal Neurology9 found that people who consume foods rich in B12 may reduce their risk of Alzheimer’s in their later years. For each unit increase in the marker of vitamin B12, the risk of developing Alzheimer’s was reduced by two percent. Remember, sublingual methylcobalamin may be your best bet here.

Watch the video discussion.URL:

Quotes For When You Can’t Decide

It can sometimes feel paralyzing to have to make decisions of any kind. Big ones or small ones, they all can seem impossible sometimes. The thing is, though, if we don’t make any decisions we will end up stuck in the same place we always are – and without making decisions for ourselves, that isn’t a very great place. Kind of ends up feeling like purgatory.But something that I have come to learn is that it is very rare you make a decision you can’t come back from. And the great thing about choices is that you can always make another one if one doesn’t work the way you wanted.

1. Mixed feelings are the worst.
“I could settle down, but I can’t settle.” 

2. Sometimes, it is okay to admit to yourself that it isn’t the right time for you to decide on anything.

“They say follow your heart, but when [your] heart is in so many pieces, which way are you to follow?” 

3. It is hard when there are so many things to think about.

“I’m indecisive because I see eight sides to everything.” 

4. Sometimes the hardest part is understanding what is going to be important.

“The problem, simply put, is that we cannot choose everything simultaneously. So we live in danger of becoming paralyzed by indecision, terrified that every choice might be the wrong choice.” 

5. Never let this happen.

“Indecision becomes decision with time.” 

Is There a Link Between Space Weather and Animal Beachings? Researchers Launch Study to Find Out.

Powerful geomagnetic storms that erupt in outer space have been known to cause disruptions to power grids, radio communication and satellites that orbit Earth.

But could space weather also have an impact on the navigational abilities of certain marine animals?

In February, it was announced that researchers from the Bureau of Ocean Energy Management (BOEM) and International Fund for Animal Welfare (IFAW) would combine with NASA on a study that would examine how solar storms may impact the internal compasses for certain species.

Antti Pulkkinen, a NASA heliophysicist who will co-author the study, provided several theories on why space weather conditions may result in healthy whales, dolphins and porpoises, collectively known as cetaceans, washing ashore.

The growing problem of co-treatment with opioids and benzodiazepines.

A powerful example of potentially dangerous low value care

Since 1999, the US has witnessed a fourfold increase in deaths from overdose involving prescription opioids,1 a fact widely known by US residents. That benzodiazepines are present in over 30% of overdoses involving prescription opioids is less well known.2

Using claims based data from 315 428 privately insured individuals in the US with at least one filled prescription for an opioid in 2001-13, Sun and colleagues (doi:10.1136/bmj.j760) examined the prevalence of a hazardous prescription combination.3 The risk of combining opioids and benzodiazepines has long been understood; both drug classes can be sedating, suppress respiratory efforts, impair thought, slow response time, and increase falls.2Sun and colleagues found an alarming rise in this prescribing practice in their study population, from 9% in 2001 to 17% in 2013. They report a significantly increased risk of overdose among patients receiving both drug types concurrently, documenting one type of harm associated with this unsound and growing clinical practice.

The study emerges at a time when clinicians are increasingly engaging in dialogue about low value care—care that is not evidence based and is potentially harmful, unnecessary, or redundant.4 Attention to low value care expands existing efforts to systematically measure and improve quality of healthcare. Early quality metrics focused on errors of omission, such as missed opportunities to screen for cancer or to vaccinate; more recent initiatives target overuse of health services or errors of commission. This shift has been advanced in the US by the Choosing Wisely campaign.5In October 2016, Britain’s Academy of Medical Royal Colleges launched a similar program, Choosing Wisely UK.6 Other countries are likewise working to explicitly define low value care as a first step to reducing it.

Most definitions of overuse of healthcare focus on a single service in a specific population of patients. Common definitions of overuse related to prescription drugs identify one drug class in a narrowly defined group of patients (such as benzodiazepines prescribed to older adults for insomnia or agitation).7 Choosing Wisely lists, to date, do not include drug-drug combinations such as benzodiazepines and opioids. Hazardous treatment combinations probably represent an important and relatively common form of low value care. Such practices could serve as powerful and measureable indicators of poor quality. Hazardous drug-drug combinations could be among the most readily identifiable forms of risky treatment combinations.

Concern about concurrent use of opioids and benzodiazepines led two US government agencies to act in 2016. The Centers for Disease Control and Prevention (CDC) guidelines on opioid prescribing urge clinicians to avoid concurrent prescribing of benzodiazepines and opioids,2 and the Food and Drug Administration (FDA) now requires black box warnings (the highest level of alert) on product labels and patient focused medication guides for opioids and benzodiazepines, recognizing the adverse outcomes associated with their concurrent use.8

Warnings and guidelines, while important to defining problematic practice, are not likely to change clinical behavior, at least not quickly. Performance metrics used by payers could prove a key lever for change. In the US and the UK, payers hold clinicians and facilities accountable for basic quality. But we found no example of performance metrics targeting hazardous drug combinations. Optimal use of safety alerts in electronic health records could prove effective, but only if they appropriately notify prescribers of hazardous combinations and only if prescribers are held accountable for over-riding warnings. Guidelines provide explicit definitions of best practice, but, as with all else in healthcare, the challenge is in effective implementation and incentives sufficient to motivate changes in the system.

Although implementation of expanded quality metrics, incentives, and systems that facilitate safer prescribing practice around drug combinations will take time, Sun and colleagues provide evidence that can be of immediate use.3 For example, the risk of overdose was 71% higher in chronic users who concurrently used a benzodiazepine compared with chronic users who did not (5.36% v 3.13%). Clinicians caring for patients using opioids chronically need to be especially cautious. Research shows that opioids are prescribed by multiple providers,9 a situation more common in deaths from overdose when both opioids and benzodiazepines were being taken.2 Providers can incorporate such evidence into practice rapidly with the right systems in place.

Unless systems are set up to push information to providers, however, busy clinicians will struggle to keep up with their patients’ use of different prescriptions. For example, current state monitoring programs for prescription drugs in the US require separate computers with separate authentication, one of many reported barriers to use.

A multi-pronged effort from both regulators and experts writing clinical guidelines, along with extensive expansion in warnings about the hazards of drug-drug interactions, are essential to reduce low value, potentially dangerous care.


Censorship: Google to start flagging “offensive” content as another form of censorship.

One of the most dangerous words in America today is the word “offensive,” not because it’s used to describe something that hurts one’s feelings, but because of how it is used by the progressive Left. It goes without saying that the word “offensive” is a subjective term that can mean many different things to many different people; what Sally finds offensive may not be offensive to Joe, and vice versa. Because of the term’s lack of definition, it is up to us to give it definition. This is dangerous because it invites people to use the word in a way that best suits their own biases or agendas. Such is the case with the Democratic Party, which has essentially hijacked the word “offensive,” and now uses it to mean anything that comes out of the mouth of a conservative.

Image: Censorship: Google to start flagging “offensive” content as another form of censorship

Americans should be very weary whenever they see a company or an organization announce plans to combat offensive language. Entities, just like individuals, have their own political agendas, and often justify silencing the opposition by claiming to be combating “offensive speech.”

Google is the latest corporation to join the fight against “offensive” speech on the Internet. Recently, the multibillion-dollar company directed its review teams to locate and flag language that could potentially be upsetting or offensive. By doing this, Google hopes to improve the overall quality of search results. (RELATED: Read about how Google took action to censor Natural News).

If a member of the Google review team decides that one of the search results contains racial slurs, or that it promotes hate or violence in some way, then the content will be flagged under a new “upsetting-offensive” category.

While the flagging system doesn’t delete search results completely, it does make it so that “offensive” results are buried and made more difficult to find, whereas search results that are considered to be high quality are more easily accessible. For example, an article about the role the religion of Islam plays in terror attacks may be pushed down and made more difficult to find, while an article about celebrating diversity would be a “quality” search result and found more easily. This, of course, is an extreme example, but you get the point.

The review teams that are responsible for judging the quality of the search results are called “quality raters.” These people examine different websites and other content to look for things that are offensive or upsetting, such as pornography. The new feature that Google has added gives these quality raters the ability to list the “offensive content” under the new “upsetting-offensive” category. Thus far, Google has declined to comment on these changes.

The “upsetting-offensive” flag reportedly instructs reviewers to “flag to all web results that contain upsetting or offensive content from the perspective of users in your locale, even if the result satisfies the user intent.” In other words, even if the results satisfy what the user was searching for, such as white supremacist websites or anti-Semitic articles, they could still potentially get flagged, even though it still wouldn’t delete the search result entirely.

While an excess of propaganda and misinformation circulating the web is not something that should be encouraged, any company that seeks to regulate speech should instantly raise the red flag for supporters of the First Amendment. While it appears that right now Google is only seeking to limit the amount of extreme content out there, such as pornography and white supremacist sites, this new initiative could easily begin infringing on the free speech rights of American citizens, even if it’s speech that is not offensive or upsetting. Despite good intentions, Google may very well have started down a slippery slope.

If you are uncomfortable or weary about what Google is doing, sign our petition to let them know that their actions are in violation of the First Amendment’s freedom of speech.


This Muslim Olympic athlete has an important message about the Nike hijab.


Nike are launching their first Muslim sportswear headscarf, the Nike Pro Hijab – and the response was vocal, to say the least.



According to a Nike statement:

​The Nike Pro Hijab has been a year in the making, but its impetus can be traced much further back to Nike’s founding mission, to serve athletes, with the signature addendum: If you have a body, you’re an athlete.

But one voice emerges from the discourse as somewhat more relevant: that of Amna Al Haddad, Olympic weightlifter from the UAE.

Along with figure skater Zahra Lari, 27-year-old Al Haddad actually tested the product, which is due to be launched in 2018.

In response to the online furore, the six-time gold medallist shared a statement on her Facebook and Instagram, along with a powerful picture:


It surely will encourage a new generation of athletes to pursue sports professionally, and without us athletes who fought for this right and made it happen, Nike wouldn’t “just do it”.

Al Haddad told FEMAIL:

I felt that people were confused by the launch and I was inspired to raise awareness that with such a product Nike isn’t dismissing anyone else’s previous work, or oppressing women, that it is simply including Muslim female athletes who require such a product.

It’s an expansion and a beautiful one that Nike is becoming a well-rounded brand that caters to everyone and all sports.

7 Ways Cannabis Can Protect The Brain.

Cannabis kills brain cells, right? Think again…

It’s true, most of us can think of at least one committed stoner with a memory of a goldfish and a vacant, thousand yard stare. So it may seem counter-intuitive to suggest that the cannabis plant can actually protect the brain and prevent certain neurodegenerative diseases like Alzheimer’s from forming.

And yet, even though the US government officially denies any such therapeutic use of cannabis, it has taken out a patent on cannabinoids saying they ‘are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia’.

So, instead of damaging memory it would seem that cannabis could actually do quite the opposite, and even protect against age related memory loss and dementia.

The Endocannabinoid System (ECS) – a therapeutic target:

Scientists have known for some time that the body’s Endocannabinoid System – the complex network of chemical compounds and receptors found throughout the central nervous (CB1) and the immune system (CB2) – is directly involved in the mechanisms of diseases like Alzheimer’s and Parkinson’s.  An increased CB2 expression (1) found in post-mortem brains Alzheimer’s patients has been thought to be the ECS’s attempt to counteract the chronic inflammation found in the disease, while in another study (2) on Alzheimer’s patients, reduced levels of the endocannabinoid anandamide were found, although conversely were elevated in Parkinson’s disease (3).

Researchers believe then that by targeting the Endocannabinoid system, therapeutic answers can be found for many of the neurodegenerative diseases affecting people in the 21st century. And much research is being carried out into how phytocannabinoids like THC and CBD can not only treat disease progression, but also even prevent certain neurodegenerative disorders from happening.

So why exactly is cannabis being posited as the brain protector of the future?

1. Cannabis protects the brain by reducing inflammation

It’s commonly held that chronic inflammation is at the root of many illnesses, including Alzheimer’s. Although it still remains unclear whether inflammation is a by product or a direct contributing factor, bringing an excessive inflammatory response into balance again, is generally believed to be of benefit.

Gary Wenk, PhD, professor of neuroscience, immunology and medical genetics at Ohio State University, has studied how to combat brain inflammation for over 25 years. He says, ‘PET imaging studies of humans have shown that after age thirty the brain gradually displays increasing evidence of inflammation. With advancing age, brain inflammation continues to worsen leading to a decline in the production of new neurons, called neurogenesis, that are important for making new memories’.

He coined the phrase ‘one puff is enough’ after suggesting that ingesting small amounts of cannabis over years can be enough to protect the brain against inflammation, saying ‘the evidence available from studies of humans and animal models of Alzheimer’s disease do indicate that long-term, low-dose daily exposure, during mid-life, to the complex blend of compounds found in the marijuana plant can effectively slow the brain processes underlying Alzheimer’s disease’.

2. Cannabis is a powerful antioxidant protecting against toxic build up in the brain

As well as patenting Cannabinoids as neuroprotectants, the US government also named them antioxidants. But the two qualities are indelibly linked.

An ageing brain has a tendency to accumulate excessive levels of glutamate, a neurotransmitter that is involved with nerve cell signalling. This can lead to glutamate toxicity, an overstimulation of the cell and ultimately cell death. When glutamate causes cellular damage, it becomes an excitotoxin. Excitotoxicity is viewed as a potential cause of many neurodegenerative diseases of the central nervous system, as well as strokes and hearing loss.

In one study (4) carried out on rats, the cannabinoid Cannabidiol was ‘was demonstrated to reduce hydroperoxide toxicity in neurons. In a head to head trial of the abilities of various antioxidants to prevent glutamate toxicity, cannabidiol was superior to both alpha-tocopherol and ascorbate in protective capacity.’  And in another, (5) THC was shown to reduce the levels of glutamate in the brain following a traumatic brain injury.

An additional age related toxicity that researchers believe may bring about the onset of diseases like Alzheimer’s and Parkinson’s is excessive levels of iron in the body.

Researchers from Pontifical Catholic University in Brazil (6) examined the relationship between high levels of iron and cell death in neurodegenerative diseases. In particular they studied the potential use of CBD, which they found may protect the rapid cell death associated with iron.

3. Cannabis helps promote new brain cell growth

7-ways-cannabis-can-protect-the-brain-1This is the one that really stops people in their tracks. Surely cannabis kills off brain cells, right? While it’s true in young, adolescent brains, cannabis can have a negative effect on brain development, scientists do know that the Endocannabinoid system is closely linked with the process of adult neurogenesis (brain cell growth).

Once again mice were the subjects of research (7) that showed the administration of plant cannabinoids promoted hippocampal neurogenesis – new cell growth in the region of the brain associated both with memory and learning – but also depression and anxiety.

In a follow on study (8) by the University of Saskatchewan, researchers sought to find out whether this hippocampal neurogenesis could explain the apparent anti anxiety and antidepressant effects of cannabinoids. Using a synthetic cannabinoid called HU-210 on rats, they found it gave rise to both the growth of ‘newborn neurons’ in the hippocampal area but also reduced anxiety and depression like behaviour in the animal subjects.

Thus showing that ‘cannabinoids appear to be the only illicit drug whose capacity to produce increased hippocampal newborn neurons is positively correlated with its anxiolytic- and antidepressant-like effects’.

4. Cannabis may slow the progression of some neurodegenerative diseases

We’ve seen that cannabis can potentially be a neuroprotector, but what effect does it have on slowing the progress of illnesses related to the brain and central nervous system?

So far, as generally is the case with research into the use of cannabis to treat disease, most findings are at the pre-clinical stage on animal models, or in the laboratory.

One such trial (9) has shown how CBD can reduce neural inflammation in mice injected with amyloid-beta, the protein that scientists believe leads to neuronal cell death in Alzheimer’s.

Research (10) carried out in 2014 at the University of South Florida showed that extremely low doses of THC actually reduces amyloid-beta production. “THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer’s pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function,” said study lead author Chuanhai Cao, PhD of the study.

By increasing mitochondrial function it also means a healthier brain due to a better energy supply and improved signalling.

5. Cannabis can make Alzheimer’s patients less agitated

A small amount of clinical trials have taken place on Alzheimer’s patients using cannabinoids to lessen levels of agitation.

One double-blind, placebo-controlled, six-week, crossover study of 12 patients suffering from Alzheimer-type dementia reported that 5 mg of dronabinol (delta 9-THC) daily was associated with a decrease in disturbed behaviour (11).

A recent study (12) carried out on 11 patients in Israel found that out of the 10 patients that completed the trial ingesting medical cannabis oil, researchers recorded “significant reduction” in behavioural and psychological symptoms of dementia. Researchers concluded that ‘adding medical cannabis oil  to Alzheimer’s patients’ pharmacotherapy is safe and a promising treatment option’.

6. Cannabis may protect the brain against serious brain trauma

5.3 million people live with traumatic brain injury (TBI) in the US, a number comparable to those living with Alzheimer’s. It is caused by a severe blow to the head and resulting symptoms can include cognitive problems such as headache, difficulty thinking, memory problems, attention deficits, mood swings and frustration.

TBI is also proving an exciting area of research for the potential therapeutic use of cannabinoids. THC in particular has been shown to protect the brain from long term damage following a traumatic injury. In a study (13) carried out on mice by Professor Yosef Sarne of Tel Aviv University, very low doses of THC administered over a long period of time were found to ‘protect the brain from long-term cognitive damage in the wake of injury from hypoxia (lack of oxygen), seizures, or toxic drugs’.

Not only did they find that THC minimised the damage to the brain following an injury, but if administered before the incident it could prevent brain injury from occurring in the first place. It seems strange to suggest taking THC just in case a brain trauma might occur, but in instances such as major surgery when blood supply to the brain is interrupted, THC’s neuroprotection could be of benefit.

This theory appears to be backed up by a study (14) carried out at a hospital in California reviewing the data of 446 adults treated for brain injuries. Overall 1 in 5 patients tested positive for THC and compared to the patients who hadn’t tested positive, they were statistically 80% less likely to die from their injuries.

While this doesn’t demonstrate a direct cause and effect between THC use and survival from serious brain trauma, the findings certainly highlight the potential use of cannabinoids for giving the best chances of recovery.

7. Cannabis could limit brain damage resulting from strokes

7-ways-cannabis-can-protect-the-brain-strokeWhereas a TBI is caused by an external force injuring the brain, a stroke occurs when due to a thickening of the arteries, there is poor blood flow to the brain, resulting in cell death, partial paralysis etc.

Scientists are slowly beginning to realise how the endocannabinoid system is activated during a stroke (15) whereby ‘activation of the CB receptors leads to cellular changes that are extremely relevant to ischemic injury (stroke damage): they regulate glutamate release, nitric oxide synthesis, growth factor expression, cellular antioxidant activity, the release of inflammatory cytokines, and leukocyte adhesion to cerebral vessels.’

Both CBD and THC’s ability to block the neurotransmitter glutamate, produced when the brain is deprived of oxygen, once again come to the fore as a way to limit cell death following a stroke. In a study (16) published in 2010 scientists concluded that ‘CBD had a potent and long-lasting neuroprotective effect and prevented progressive post-ischemic injury’ and ‘that repeated treatment with CBD from 1 day or 3 days after cerebral ischemia improved the functional deficits, such as neurological score and motor coordination, and survival rates’.

Another rodent study (17) showed Cannabidiol to have ‘a protective effect on neuronal death induced by ischemia (stroke)’ indicating that it ‘might exert beneficial therapeutic effects in brain ischemia’.

So contrary to the commonly held belief that cannabis leads to the loss of precious neurones, studies increasingly show the potential benefits for protecting our ageing brains against neurodegeneration and even injury from external forces.

It’s clear that there is a lot still to understand about the endocannabinoid system’s role in these particular diseases, but scientists remain hopeful that the many theories honed in the lab may one day move forward into the realms of clinical trials, and eventually to treatment for patients.


  1. Solas M1, Francis PT, Franco R, Ramirez MJ (2013). CB2 receptor and amyloid pathology in frontal cortex of Alzheimer’s disease patients. Neurobiol Aging. 2013 Mar;34(3):805-8.
  2. Kwang-Mook Jung,a,1 Giuseppe Astarita,a,1 Sevil Yasar,d Vitaly Vasilevko,c David H. Cribbs,c Elizabeth Head,c,2 Carl W. Cotman,c and Daniele Piomelli (2012). An amyloid beta 42-dependent deficit in anandamide mobilization is associated with cognitive dysfunction in Alzheimer’s disease.Neurobiol Aging 2012 Aug; 33(8): 1522–1532.
  3. Pisani V1, Moschella V, Bari M, Fezza F, Galati S, Bernardi G, Stanzione P, Pisani A, Maccarrone M. (2010) Dynamic changes of anandamide in the cerebrospinal fluid of Parkinson’s disease patients. Movement Disorders.15;25(7):920-4.
  4. Hampson AJ1, Grimaldi M, Lolic M, Wink D, Rosenthal R, Axelrod J.(2000) Neuroprotective antioxidants from marijuana. Annals of the New York Academy of Sciences 899:274-82.
  5. Esther Shohami, Ayelet Cohen-Yeshurun, Lital Magid, Merav Algali, and Raphael Mechoulam (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology.  163(7): 1402–1410
  6. Vanessa Kappel da Silva, Betânia Souza de Freitas, Arethuza da Silva Dornelles,Laura Roesler Nery, Lucio Falavigna,Rafael Dal Ponte Ferreira, Maurício Reis Bogo, Jaime Eduardo Cecílio Hallak, Antônio Waldo Zuardi, José Alexandre S. Crippa, Nadja Schröder (2014) Cannabidiol Normalizes Caspase 3, Synaptophysin, and Mitochondrial Fission Protein DNM1L Expression Levels in Rats with Brain Iron Overload: Implications for Neuroprotection. Molecular Neurobiology. Volume 49, Issue 1, pp 222–233
  7. Jin K1, Xie L, Kim SH, Parmentier-Batteur S, Sun Y, Mao XO, Childs J, Greenberg DA. (2004) Defective adult neurogenesis in CB1 cannabinoid receptor knockout mice. Molecular Pharmacology. 66(2):204-8.
  8. Jiang W1, Zhang Y, Xiao L, Van Cleemput J, Ji SP, Bai G, Zhang X (2005). Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.The Journal of Clinical Investigation. (11):3104-16.
  9. G Esposito, C Scuderi, C Savani, L Steardo, Jr, D De Filippis, P Cottone, T Iuvone, V Cuomo, and L Steardo (2007). Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1? and iNOS expression. British Journal of Pharmacology. 151(8): 1272–1279
  10. Cao C, Li Y, Liu H, Bai G, Mayl J, Lin X, Sutherland K, Nabar N, Cai J. (2014) The potential therapeutic effects of THC on Alzheimer’s disease. Journal of Alzheimer’s Disease 42(3):973-84
  11. Volicer, L., Stelly, M., Morris, J., McLaughlin, J. and others. (1997). Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer’s disease. Int.J.Geriatr.Psychiatry. 12: 913-919.
  12. Shelef A, Barak Y, Berger U, Paleacu D, Tadger S, Plopsky I, Baruch Y. (2016) Safety and Efficacy of Medical Cannabis Oil for Behavioral and Psychological Symptoms of Dementia: An-Open Label, Add-On, Pilot Study. Journal of Alzheimer’s Disease. 51(1):15-9
  13. Fishbein M, Gov S, Assaf F, Gafni M, Keren O, Sarne Y. ( 2012) Long-term behavioral and biochemical effects of an ultra-low dose of delta 9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling. Experimental Brain Research. 221(4):437-48
  14. Nguyen BM, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. (2014) Effect of marijuana use on outcomes in traumatic brain injury. American Surgeon. Oct;80(10):979-83.
  15. Cecilia J. Hillard (2008) Role of cannabinoids and endocannabinoids in cerebral ischemia. Current Pharmaceutical Design 14(23): 2347–2361.
  16. Kazuhide Hayakawa, Kenichi Mishima, and Michihiro Fujiwara (2010). Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke. Pharmaceuticals 3(7): 2197–2212.
  17. Schiavon AP, Soares LM, Bonato JM, Milani H, Guimarães FS, Weffort de Oliveira RM.(2014) Protective effects of cannabidiol against hippocampal cell death and cognitive impairment induced by bilateral common carotid artery occlusion in mice. Neurotoxicity Research 26(4):307-16


Do Happiness Interventions Really Work?

Cannabis Compound Found to Remove Toxic Alzheimer’s Protein From the Brain.

Alzheimer’s is a major problem, and as Americans continue to age, it’s becoming an increasing one. But what if cannabis had the answer?

According to Real Farmacy, cannabis is the answer – as a compound (THC, more specifically) can remove toxic amyloid beta protein clumps, which some believe are responsible for Alzheimer’s disease, from the brain.
Marijuana enthusiasts the world over are already rejoicing, simply because they heard THC. Smoke ’em if you got ’em?
Researchers are suggesting that THC works to fight Alzheimer’s by clearing those protein clumps, thereby decreasing the likelihood of the lesions some researchers believe are responsible for Alzheimer’s.
In 2006, researchers at the Scripps Research Institute found that THC inhibits the formation of amyloid plaques by blocking the enzyme in the brain that produces them. Schubert and his team have found that THC is also able to eliminate a dangerous inflammatory response from the nerve cells, thus ensuring their survival.

So far, Schubert and his team have only tested THC on neurons in a lab. Their next step will be to observe the link between THC and reduced inflammation and plaque build-up in a clinical trial.

THC is a popular word among marijuana enthusiasts because it is responsible for the majority of marijuana’s psychological effects, including the high. THC has natural pain-relieving properties, and is effective in treating symptoms for everything from stroke and chemotherapy to chronic pain, post traumatic stress disorder, and HIV.

When consumed, THC passes from the lungs to the bloodstream, and attaches itself to two different types of receptors, cannabinoid receptor (CB) 1 and 2. These receptors are found on cell surfaces all over the body.

Receptors in the brain are most concentrated in neurons associated with pleasure, memory, thinking, coordination, and time perception. These receptors usually bind with a class of lipid molecules called endocannabinoids that are produced by the body during physical activity to promote cell-to-cell signaling in the brain.

THC can also bind to these lipid molecules in the same way. When THC does this, it begins to mess with the brain’s ability to communicate with itself. This can be both a good and a bad thing.

Research suggests that by binding to these receptors, THC could actually have a positive effect on aging brains because it can help the body clear out toxic accumulations of amyloid beta.

While no one is 100% sure of what causes Alzheimer’s disease, it is thought to be the result of a build-up of two types of lesions: amyloid plaques and neurofibrillary tangles.

Amyloid plaques are dense clusters of beta-amyloid molecules that sit between neurons. Neurofibrillary tangles are caused by defective tau proteins that clump up into a thick, insoluble mass in the neurons.

It is still unclear why these lesions begin appearing in the brain, but studies have linked inflammation in the brain tissue to the build up of plaques and neurofibrillary tangles. According to these studies, something that is capable of easing brain inflammation while simultaneously encouraging the body to clear out these lesions could become the first effective treatment for Alzheimer’s.

Turning down your heat could improve your life

My dearest wish is to one day have the pleasure of living in a small cabin in the frigid wilderness.

There I will spend my nights covered in heavy wool blankets, eating smoked fish and dried fruit.

Over time, my beard will grow to the point where I’ll be indistinguishable from a medium-sized woodland creature.

The villagers I’ll come to know during my rare visits to town will call me “the wolfman,” not least because I will communicate solely by howling and scratching out messages with my clawlike fingernails.

For now, I live in a big city, where such unconventional grooming habits are frowned upon, but I make a point of using very little heat.

 cold weather

I’ve suffered for living the no-heat lifestyle. Friends will come to my apartment from time to time and ostentatiously shiver, as if to tell me that I am somehow letting them down by not swaddling them like newborns in a pillowy bosom of artificial heat.

There are times when I’ve been tempted to fill my bathtub with molten lava. If you like artificial heat so much, I say to them in my imagination, why not soak in this magma bath?

Though it is not my job to tell you how to live — I respect you too much for that — I urge you to at least consider turning down your thermostat too.

I ask you not because of the devastating environmental consequences that flow from your heat addiction. I know you well enough to know that you don’t give a damn about this planet we call home, which you routinely defile with your candy bar wrappers and the greenhouse gases that belch from the airplanes you love to fly.

Instead, I will appeal to your selfishness, you heat-loving scalawags. All of that heating oil, natural gas, and firewood you’re burning up is sapping you of your emotional, spiritual, and physical well-being.

To my lasting dismay, Americans routinely heat their living rooms to 70 degrees Fahrenheit, and their bedrooms to a balmy 68 degrees. That anyone can sleep in such temperatures boggles the mind.

It is a minor miracle that US homes aren’t being overrun by lush tropical plants, even in the dead of winter. What is it that you people are doing at these temperatures? Are you stripping down to your underpants and performing ritual dances in worship of Ra, the sun god of ancient Egypt, even as snow falls outside?

That I can understand, and indeed I’ve been known to indulge in a bit of Ra worship myself every now and again. But surely this is not an every-night activity. Are you grilling Italian sausages on top of your radiators? As delicious as this sounds, it is generally best to grill such protein-rich delights in the device George Foreman builds expressly for this purpose.

Are you slow-roasting yourselves for the benefit of the wandering ogres who will one day devour you? Fair enough. Yet you should know that your average ogre prefers to eat his humans al dente.

Granted, there are some for whom lower temperatures are simply intolerable. My parents, for example, were born and raised in a semitropical part of the world, and they find the cold hard to bear. Having been raised by heat-lovers, it took me a while to fully adapt to the no-heat lifestyle.

At first I’d turn down the thermostat and bundle up. When I’d lounge around my apartment, I’d wrap myself in multiple layers of high-tech synthetic fabrics. I’d cover my body so thoroughly that I’d look much like a bulky snow ninja, complete with balaclava.

While wearing this getup, I’d alternate between doing jumping jacks and karate-chopping the cold. Truth be told, I felt rather proud of myself. But that’s before I realized that I was cheating myself of the full benefits of going without heat. No, if you’re going to really embrace the no-heat lifestyle, you can’t wear 12 sweaters and a knit cap (a look I like to call “freezecore”) to bed. Instead, you have to turn down the thermostat … and then get naked.

There is growing evidence that shivering can transform white fat into brown fat, a transformation that appears to protect animals from diabetes and obesity. I won’t pretend to understand this strange alchemy. This “science” of yours frightens and confuses me.

My crude understanding is that while white fat simply stores energy, brown fat burns energy to keep us from turning into popsicles. The more time we spend in artificially hot environments, the more our brown fat deposits just wither away.

One result is that we grow plumper, and more vulnerable to all manner of maladies. You don’t have to shiver to activate your brown fat deposits. Simply lowering the thermostat to, say, 60 degrees will keep your brown fat active.

So no, I’m not telling you to let indoor temperatures fall below zero, or to allow your pipes to freeze and burst. That would be foolish. Rather, I am urging you to endure uncomfortably low temperatures.

Potential health benefits aside, the no-heat lifestyle will put you in touch with the rhythms of the natural world. Winter is with us for a few months at most. Why not lower your defenses and savor it?

Instead of turning up the heat, you ought to eat more soup. Let the brown fat deposits build. Invite the snowperson you’ve built in your backyard to move in, and to pay her share of the rent. Let the cold chisel away your weakness, leaving behind a lean, wolflike creature ready to take a bite out of life. You will thank me later.


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