Berries for Inflammation and Osteoarthritis Treatment

How might berries improve human health, healthy aging, and quality of life?  Maybe, due to their anti-inflammatory effects, since inflammation can be an underlying contributing factor in the “development, progression, and complication” of a number of chronic diseases. Higher intake of anthocyanins, the brightly-colored pigments in berries, has been associated with anti-inflammatory effects, which may be “a key component” underlying the associated reduction in chronic disease risk. But these are all just associations. You can’t prove cause and effect until you put it to the test.

A double-blind, randomized, placebo-controlled trial found that blueberry smoothies could turn off inflammation genes. (This is measuring the expression of pro-inflammatory genes in white blood cells taken from individuals before and after six weeks of drinking placebo smoothies with no blueberries.) They got worse over time. Six weeks later, more inflammatory chemicals pouring out, whereas the blueberry group started out about the same at week zero, but six weeks of daily blueberries and, the expression of inflammatory genes went down.

“In addition to attenuating inflammation,” they demonstrate that “blueberry consumption was able to significantly decrease the levels of free radicals” in their bloodstream: no change in the placebo group, but after six weeks of blueberry smoothies, the amount of free radicals in their blood was  extinguished by half. Okay, but does all that antioxidant and anti-inflammatory power actually translate into clinical benefits? For example  what is the effect of blueberry consumption on recovery from excessive weight lifting-induced muscle damage?

A randomized crossover study: a blueberry smoothie or antioxidant-matched placebo smoothie five and 10 hours prior to, and then 12 and 36 hours after, exercise-induced muscle damage. The smoothies were about a cup and a half of frozen strawberries, a banana, and apple juice, or without the berries, but dextrose and vitamin C added to match it for calories and antioxidant power. Even so, the blueberries worked better at mopping up free radicals. Here’s the oxidative stress without the blueberries: it goes up and stays up. But, with the blueberries, it comes right down. Yeah, but what we care about is the recovery of muscle strength, so you can jump right back into training. Same drop in peak torque 12 hours later, but a day later, significantly faster restoration of peak muscle strength, demonstrating that the ingestion of blueberries can accelerate recovery — something that may be especially relevant to athletes who compete over successive days.

That’s all well and good, but what about using berries to treat inflammatory diseases like arthritis?  Yes, they may have protective effects against arthritis in a rat — significantly reducing “paw volume”— how swollen their paw gets when you inject it with some inflammatory irritant. But there had never been any human arthritis berry studies, until now.

Remember that amazing study where strawberries alone could reverse the progression of precancerous lesions? The strawberries were dramatically downregulating pro-inflammatory genes. Give strawberries to diabetics for six weeks, and not only does their diabetes get better, their C-reactive protein levels, a marker of systemic inflammation, drops 18%. Even just a single meal can help. Have people eat a largely unhealthy breakfast, and the level of inflammatory markers goes up over the next six hours, but less so if you added just five large strawberries to the meal.

So, can “strawberries improve pain and inflammation” in confirmed knee osteoarthritis? No fair that the title ruined the suspense, but yes, osteoarthritis patients randomized to get like a pint and a half of strawberries a day for 12 weeks and yeah, certain inflammatory markers plummeted on the strawberries. But did they actually feel any better? Significant reductions in constant pain, intermittent pain, and total pain. The “first clinical study on the effects of…berries” on human arthritis, and found that a “simple dietary intervention, the addition of berries to one’s diet, may have a significant impact on pain, inflammation, and overall quality of life in obese adults with [osteoarthritis].”


Why Do Plant-Based Diets Help Rheumatoid Arthritis?

Rheumatoid arthritis is a chronic systemic autoimmune disease affecting millions, characterized by persistent pain and stiffness, and progressive joint destruction—particularly in the hands and feet, leading to crippling deformities. What can we do to prevent it and treat it?

In a famous 13-month long randomized controlled trial of plant-based diets for rheumatoid arthritis, patients were put on a vegan diet for three and a half months, and then switched to an egg-free lactovegetarian diet for the remainder of the study. Compared to the control group, who didn’t change their diet at all, the plant-based group had a significant improvement in morning stiffness within the first month, cutting the number of hours they suffered from joint stiffness in half. Pain dropped from five out of ten down to less than three out of ten. A drop in disability; they reported subjectively feeling better, significant improvement in their grip strength, fewer tender joints, less tenderness per joint, and less swelling, with the added benefit of losing about 13 pounds and keeping most of that weight off throughout the year. They also had a drop in inflammatory markers in their blood, sed rate, C-reactive protein, and white count. The question is why. What does diet have to do with inflammatory joint disease?

Well, rheumatoid arthritis is an autoimmune disease in which your body attacks the lining of your own joints. Why would it do that? Well, there’s a different autoimmune disease called rheumatic fever, in which your body attacks your own heart. Again, why would your body do that? It appears to be a matter of friendly fire.

Rheumatic fever is caused by strep throat, which is caused by a bacteria that has a protein that looks an awful lot like a protein in our heart. So when our immune system attacks the strep bacteria, it also attacks our heart valves, triggering an autoimmune attack by “molecular mimicry.” The protein on the strep bacteria is mimicking a protein in our heart, so our body gets confused and attacks both. That’s why it’s critical to treat strep throat early to prevent our heart from getting caught in the crossfire.

So researchers thought maybe rheumatoid arthritis might be triggered by an infection as well. A clue to where to start looking was the fact that women seem to get rheumatoid arthritis three times more frequently than men. What type of infection do women get more than men? Urinary tract infections, so researchers started testing the urine of rheumatoid arthritis sufferers, and lo and behold found this bacteria called Proteus mirabilis. Not enough to cause symptoms of a UTI, but enough to trigger an immune response. And indeed, there’s a molecule in the bacteria that looks an awful lot like one of our own molecules in our joints, so anti-Proteus antibodies against the bacteria may inadvertently damage our own joint tissues, leading eventually to the joint destruction. Therefore, therapeutic interventions aimed at the removal of this bacteria from the bodies of patients, with consequent reduction of antibodies against the organism, should lead to a decrease in inflammation.

Well, as we saw before, urinary tract infections originate from the fecal flora; the bugs crawl up from the rectum into the bladder. And so, how might one change the bugs in one’s colon? By changing our diet. Some of the first studies over 20 years ago on trying to fundamentally shift people’s gut flora were done using raw vegan diets, figuring that’s about as fundamental a shift from the standard Western diet as there is. And indeed, within days one could significantly change someone’s gut flora. And you put rheumatoid arthritis sufferers on that kind of diet, and they experienced relief, and the greater improvements were linked to greater changes in their gut flora. But the diet was considered so intolerable that half the patients couldn’t take it and dropped out–perhaps because they were trying to feed people things like buckwheat-beetroot cutlets buttered with a spread made out of almonds and fermented cucumber juice.

Thankfully, regular vegetarian and vegan diets work too, changing the intestinal flora and improving rheumatoid arthritis, but we didn’t specifically have confirmation that plant-based diets brought down anti-Proteus antibodies, until now. Those who responded to the plant-based diet showed a significant drop in anti-Proteus mirabilis antibodies compared to the control group. Maybe it just dropped immune responses across the board? No, antibody levels against other bugs remained the same, so the assumption is that the veg diet reduced urinary or gut levels of the bug.

A shift from an omnivorous to a vegetarian diet has a profound influence on the composition of the urine–for example, higher levels of lignans in the urine of those eating vegetarian. Up until now, it was just thought that lignans protected people eating more plant-based from getting cancer, but now we know lignans can also have antimicrobial properties as well, so may be helping to clear Proteus from the system. Either way, this suggests a new type of therapy for the management of rheumatoid arthritis. This new treatment includes anti-Proteus measures such as dietary manipulations in the forms of vegetarian diet.


A New (Old) Treatment for COVID-19



Pandemic COVID-19.  What can/should we do?

Having reached nearly 1.8 million reported cases globally, with reported deaths of nearly 110,000 this pandemic is reaching all corners of the globe and affecting all sections of society.

The impact on each population is profoundly affected by the decisions made by local and federal governments to promote handwashing and early social distancing and the extent to which a society is able to comply with that.  The ultimate solution to the pandemic, an effective vaccine is 12-18 months away. At the other end of the clinical course, hospital and ICU staff are either struggling to find adequate PPE, beds, ventilators and new treatments to minimise the substantial morbidity and mortality or preparing for the surge in clinical needs depending on where their city is in the course of the spread of the virus.  The resources that are able to be amassed to fight end stage COVID-19 are vastly different depending on the health system of the country affected.  

COVID-19 has a known clinical course (with the obvious variation of asymptomatic carriage). On average around day 5 become symptomatic, get tested (if testing available in patients region), then go home to wait and see what happens.  If they are lucky they become one of the 80% who recover without hospitalisation or if not, around day 12, they will need to go into a hospital with resources stretched beyond capacity, and will have significantly worse morbidity and mortality.  There is no active treatment in this middle stage of the clinical course, the outcome of which predominantly depends on whether their innate immune function is able to overcome SARS CoV-2’s direct impairment. Fever is well known to enhance innate and adaptive immunity.  

In Newcastle, Australia, we are proposing research into whether heat applied to the body as a proxy for fever can alter the clinical course of COVID-19 and decrease the likelihood of hospitalisation and poor clinical outcomes.  This sort of research is incumbent upon clinicians and countries that have the wherewithal, to support the global fight against COVID-19. In other countries, clinicians may choose to act on biological plausibility and clinical imperative alone.

Immune Pathophysiology of Coronaviruses causing SARS, MERS and COVID-19

Coronavirus infections that result in SARS, MERS and COVID-19 show the viruses are able to actively impair the innate immune response, in particular the Type 1 interferon (IFN) response from infected cells (such as Type 2 alveolar cells and likely macrophages and T cells).  They also (either directly or as a result of decreased IFN Type 1) impair monocytes and other innate immune cells (eg natural killer cells) which are required to phagocytose virus and present it to lymphocytes to switch on adaptive immunity [1-3].  

…excessive type I IFN with the infiltrated myeloid cells are the main cause of lung dysfunction and negatively impact the outcome of the infection. It is speculated that upon SARS-CoV or MERS-CoV infection, delayed type I IFN compromises the early viral control, leading to influx of hyperinflammatory neutrophils and monocytes-macrophages. The increases in these innate immune cells yields deteriorating consequences to infected host that manifested in lung immunopathology, including pneumonia or acute respiratory distress syndrome. In SARS-CoV-2 infection, similar scenario is expected with varying degree of immune interference. Interestingly, transmission of virus is reported to occur even in asymptomatic infected individuals. This may be indicative of delayed early response of the innate immune response. Based on the accumulated data for previous coronavirus infection, innate immune response plays a crucial role in protective or destructive responses and may open a window for immune intervention. Active viral replication later results in hyperproduction type I IFN and influx of neutrophils and macrophages which are the major sources of pro-inflammatory cytokines. With similar changes in total neutrophils and lymphocytes during COVID19, SARS-CoV-2 probably induces delayed type I IFN and loss of viral control in an early phase of infection. Individuals susceptible to CoVID19 are those with underlying diseases, including diabetes, hypertension, and cardiovascular disease.2 In addition, no severe cases were reported in young children, when innate immune response is highly effective. These facts strongly indicate that innate immune response is a critical factor for disease outcome. [2]

Eighty percent of patients are able to overcome this direct innate immune suppression by the virus, mount a reasonable innate (and consequently a good adaptive) immune response and clear the virus. In about twenty percent of patients (predominantly those with impaired immunity to start with, for example – from age or obesity and it’s consequent diseases) this direct inhibition by the virus results in it being able to replicate relatively unchecked in the early days of the infection.  A few days to a week later, the body is confronted with large amounts of virus and there is an over exuberant immune response from the recruited neutrophils, monocytes and macrophages. The resultant hyperproduction of proinflammatory cytokines, the so-called “cytokine storm”, results in acute lung injury +/- ARDS +/- multi-organ failure +/- death [1-3]. See the diagram on the previous page.  

Early research has shown in vitro pretreatment of cells with IFN Type 1 in the days prior to infection shows a massive sustained reduction in viral replication and likely would result in a good in vivo result [4].   However IFN Type 1 is not yet an available experimental treatment. There are a number of other therapeutic trials showing promise with such treatments as vitamin C, plaquenil, zinc, even injection with natural killer cells etc but globally most patients are unable to access these as either in, or outpatients.   As for the case of the immune treatments like administered IFN or NK cells: what if we could do more than just increase one cytokine or cell line? What if we could activate the whole of the immune system?

How can we overcome immune inhibition by SARS CoV-2?

Fever is known to increase innate and acquired immune activity in multiple ways including:

  • increased release of heat shock proteins
  • increased phagocytic potential of dendritic cells and macrophages  
  • increased migration of APCs to regional lymph nodes, 
  • increased recruitment of neutrophils to lungs 
  • increased neutrophil activity
  • enhanced natural killer recruitment and activity  
  • increased numbers of lymphocytes. 

This is also true for induced hyperthermia eg  as created by injecting lipopolysaccharide (bacterial cell wall component) into mice or sitting in a warm bath for humans.[5,6] Hyperthermia not only optimises immune function it also directly inhibits viral replication [5].  Most importantly in the case of COVID-19, a number of studies have demonstrated that elevated body temperatures substantially augment Interferon Type 1 (IFNα) production/activity in response to viral infection [6-9] AND monocyte function[11] ie the immune processes that the virus directly inhibits.  By utilising induced hyperthermia to overcome the initial roadblocks that SARS-CoV-2 setup, the immune system is primed to proceed with a normal inflammatory response and clear the virus, rather than progress to inflammatory complications.

Fever is a good immune system enhancer as discussed above, however, there are two problems:  

  1. Not everyone mounts a good fever response to infection especially not the old and obese.  Immunosenescence (the decline in immune function with age, and obesity and its consequences) is mediated in part by impaired monocyte function[12,13]. 
  2. Fever is metabolically expensive with every degree of body temperature elevation requiring an increase in BMR of 10-12.5%.  

Mild hyperthermia induced by hydrotherapy potentially addresses both of these problems[5,11].

How can immune enhancement by hyperthermia help clinically?

The first week after diagnosis with COVID-19 infection is essentially being wasted at home.   If during that time we induced hyperthermia at home, with simple hydrotherapeutic techniques, we could directly stimulate the whole of the innate and adaptive immune response but in particular we may be able to partially or completely overcome the direct immune depressant effects of COVID-19 on INF and monocytes in the early days of infection.   If we are able to diminish the need for hospitalisation by even 5% of total infections that would be a 25% decrease in numbers requiring admission, substantially reducing the overstretched resources globally and will potentially save many lives. This potential treatment is even more important as an option for people in developing nations without a readily available hospital system, replete with ICU support.  

Hydrotherapy and COVID-19

Hydrotherapeutic hyperthermia can be induced in a number of ways, but one of the easiest  involves sitting in a warm to hot bath till sweaty, then having a douse of cold water to vasoconstrict the external vessels and keep the heat in, then resting in a warm bed for ½ an hour. The potential risks of this treatment include vasovagals due to vasodilation or arrhythmias induced by the cold water shock. Hydrotherapy is highly modifiable treatment   and can be performed with a patient in bed, in a chair or in a bath/shower with whatever is available to hand. It can also be adapted to suit the patients comorbidities and clinical status. Anecdotally, a physiotherapy colleague of mine has used therapeutic hyperthermia to good effect in many different situations around the globe. For example, by wrapping Karen refugees without access to any medical care, in black plastic to heat and then cooling off with a dip in the river for tropical PUO (likely Dengue or malaria).  When utilised in conjunction with standard medical care while working in a hospital in Bangkok, my colleague saw patients in hospital with Dengue fever fit to go home in 3 days when it usually took 7-10 days.

Could inducing a fever early just speed up the time to cytokine storm and not alter the clinical pathway at all?  

Reassuringly there is good evidence to suggest that early fever or induced hyperthermia plays a homeostatic role in managing the inflammatory course, and its outcomes, for good or ill. For example, thermal stress initially increases proinflammatory cytokine release from macrophages but, once they are activated, synthesis decreases. In addition, activated or “heat experienced” macrophages produce less TNF, IL6 and IL1beta in febrile temperatures, than heat inexperienced ones.[5]

What about those who are not infected but would like to optimise immune function today?  The evidence is a little less clear at a population rather than cellular level, (smaller studies, more observational, hard to blind people etc) but heat, then cold exposure has been shown to improve immune function, especially when used over longer periods [14,15,16]. 

A case report[17] followed the clinical course of a patient in Melbourne, Australia who recovered from COVID-19 after a brief hospitalisation.  There was a marked increase of adaptive immune cells around day 7, three days prior to alleviation of symptoms (still with noticeably low monocytes common to SARS CoV-2 infections).  It would be useful to have some comparative case studies showing what happens daily to the clinical course in COVID-19 with hydrotherapy. Taking a FBC at least on days 3 and 6 would show quickly whether immune suppression was taking place, or being overcome by the treatments and give a good prediction as to whether the patient was likely to need hospitalisation on day 12, or go on to make a good clinical resolution.  Case reports and historical records from when this treatment was used in the Spanish influenza pandemic suggest that the WCC should surge at day three (illustrating a rapid transition to acquired immunity) and bring about clinical resolution potentially around 4 days earlier than without hydrotherapy. 

It is worth noting that practicing Evidence Based Medicine is an excellent thing that helps keep us and our patients safe.  However during this pandemic ICUs and health care workers around the globe are just trying to figure out what works. There are no long term, multicentre RCTs to guide us at this stage, just clinical experience that guides expert opinion.  Once anecdotal evidence mounts, it is guiding smaller clinical trials and RCTs in regional centres. There are just too many lives to try to save to waste time waiting for someone else to deliver gold standard evidence. Not having an RCT to support a type of treatment is not stopping intensive care clinicians from trying any therapeutic modality that makes physiological sense and is available to hand.  I believe in this situation, primary care physicians, public health physicians and ID physicians should be following their lead. 

Treatment/Research Plans…

As we are making good progress in “flattening the curve” in Australia we have the opportunity to formally assess whether immune stimulation by mild hyperthermia from hydrotherapy can alter clinical outcomes.  Not every country or city is in our position. Some clinicians may choose to trial this old/new treatment for infectious disease without recent trials. This therapy is scientifically plausible, at little to no cost, readily available, and can be safely utilised by patients in their own homes with a little education and common sense.  Like all treatments hydrotherapy is not without risks eg falls from postural hypotension or arrythmias triggered by cold stimulation. If clinicians and patients are aware of the risks and contraindications to this therapy it can be considered on a case by case basis.

Detailed protocols, as well as precautions/contraindications, are available at  This information is based on clinical experience and historical textbooks/records of treatment of the Spanish Influenza pandemic.   These protocols, used with care, can be utilised to possibly:

  1. help keep patients out of hospital (more acute care for those who really need it) 
  2. diminish asymptomatic and presymptomatic shed in the community (slow community spread) especially in the young who are at least risk from this illness and are the most likely to share it without knowing it
  3. optimise our own immune function to help keep us all working safely as long as is required..

Author: Dr Emma Campbell BMed FRACGP



Highlighted in bold are the two most useful resources, if you only have time to look at a couple of papers.

  1. Channappanavar R, Fehr AR, Zheng J, Wohlford-Lenane C, Abrahante JE, Mack M, Sompallae R, McCray PB Jr, Meyerholz DK, Perlman S. IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes. J Clin Invest. 2019 Jul 29;130:3625-3639. doi: 10.1172/JCI126363. eCollection 2019 Jul 29. PubMed PMID: 31355779; PubMed Central PMCID: PMC6715373.
  2. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol. 2020 Mar;38(1):1-9. doi: 10.12932/AP-200220-0772. Review. PubMed PMID: 32105090.
  3. Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Semin Immunopathol. 2017 Jul;39(5):529-539. doi: 10.1007/s00281-017-0629-x. Epub 2017 May 2. Review. PubMed PMID: 28466096; PubMed Central PMCID: PMC7079893.
  4. Lokugamage KG, Schindewolf C, Menachery VD. SARS-CoV-2 sensitive to type I interferon pretreatment. unpublished.Forthcoming;
  5. Evans SS, Repasky EA, Fisher DT. Fever and the thermal regulation of immunity: the immune system feels the heat. Nat Rev Immunol. 2015 Jun;15(6):335-49. doi: 10.1038/nri3843. Epub 2015 May 15. Review. PubMed PMID: 25976513; PubMed Central PMCID: PMC4786079
  6. El-Radhi AS. Fever management: Evidence vs current practice. World J Clin Pediatr. 2012 Dec 8;1(4):29-33. doi: 10.5409/wjcp.v1.i4.29. eCollection 2012 Dec 8. Review. PubMed PMID: 25254165; PubMed Central PMCID: PMC4145646.
  7. Postic B, DeAngelis C, Breinig MK, Monto HO. Effect of temperature on the induction of interferons by endotoxin and virus. J Bacteriol. 1966 Mar;91(3):1277-81. PubMed PMID: 5929756; PubMed Central PMCID: PMC316024.
  8. Manzella JP, Roberts NJ Jr. Human macrophage and lymphocyte responses to mitogen stimulation after exposure to influenza virus, ascorbic acid, and hyperthermia. J Immunol. 1979 Nov;123(5):1940-4. PubMed PMID: 489966.
  9. Knippertz I, Stein MF, Dörrie J, Schaft N, Müller I, Deinzer A, Steinkasserer A, Nettelbeck DM. Mild hyperthermia enhances human monocyte-derived dendritic cell functions and offers potential for applications in vaccination strategies. Int J  Hyperthermia. 2011;27(6):591-603. doi: 10.3109/02656736.2011.589234. PubMed PMID: 21846195.
  10. Prow NA, Tang B, Gardner J, Le TT, Taylor A, Poo YS, Nakayama E, Hirata TDC, Nakaya HI, Slonchak A, Mukhopadhyay P, Mahalingam S, Schroder WA, Klimstra W, Suhrbier A. Lower temperatures reduce type I interferon activity and promote alphaviral arthritis. PLoS Pathog. 2017 Dec;13(12):e1006788. doi: 10.1371/journal.ppat.1006788. eCollection 2017 Dec. PubMed PMID: 29281739; PubMed Central PMCID: PMC5770078
  11. Zellner M, Hergovics N, Roth E, Jilma B, Spittler A, Oehler R. Human monocyte stimulation by experimental whole body hyperthermia. Wien Klin Wochenschr. 2002 Feb 15;114(3):102-7. PubMed PMID: 12060966
  12. Rao DV, Watson K, Jones GL. Age-related attenuation in the expression of the major heat shock proteins in human peripheral lymphocytes. Mech Ageing Dev. 1999 Feb 1;107(1):105-18. doi: 10.1016/s0047-6374(98)00143-2. PubMed PMID: 10197792.
  13. Parisi MM, Grun LK, Lavandoski P, Alves LB, Bristot IJ, Mattiello R, Mottin CC, Klamt F, Jones MH, Padoin AV, Guma FCR, Barbé-Tuana FM. Immunosenescence Induced by Plasma from Individuals with Obesity Caused Cell Signaling Dysfunction and Inflammation. Obesity (Silver Spring). 2017 Sep;25(9):1523-1531. doi: 10.1002/oby.21888. Epub 2017 Jul 14. PubMed PMID: 28707376
  14. Brenner IK, Castellani JW, Gabaree C, Young AJ, Zamecnik J, Shephard RJ, Shek PN. Immune changes in humans during cold exposure: effects of prior heating and exercise. J Appl Physiol (1985). 1999 Aug;87(2):699-710. doi: 10.1152/jappl.1999.87.2.699. PubMed PMID: 10444630.
  15. Dugue B, Lappanen E, Grasbeck R. Effect of thermal stress (sauna + swimming in ice-cold water) in man on the blood concentration and production of pro-inflammatory cytokines and stress hormones. Pathophysiology. 1998; 1001(5):149.
  16. Ernst E, Pecho E, Wirz P, Saradeth T. Regular sauna bathing and the incidence of common colds. Ann Med. 1990;22(4):225-7. doi: 10.3109/07853899009148930. PubMed PMID: 2248758.
  17. Thevarajan I, Nguyen T, Koutsakos M, Druce J, Caly L, van de Sandt C, Jia X, Nicholson S, Catton M, Cowie B, Tong S, Lewin S, Kedzierska K. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19. Nature Medicine. 2020/03; doi: 10.1038/s41591-020-0819-2



The Okinawa Diet: Living to 100

What would happen if you centered your diet around vegetables, the most nutrient-dense food group?

“The plant-based nature of the diet may trump the caloric restriction, though, since the one population that lives even longer than the Okinawa Japanese don’t just eat a 98% meat-free diet, they eat 100% meat-free. The Adventist vegetarians in California, with perhaps the highest life expectancy of any formally described population.”

Proof positive! Purpose in life connected with less infections.

IMG_0074A very fascinating study shows that higher amounts of purpose in life correlate with lower interleukin-6 (= pro-inflammatory cytokine) levels. In addition it reveals that educational degrees stop playing a relevant role as soon as a certain amount of purpose in life is reached.

What’s your purpose in life?


Four Nuts Once a Month

Doctor’s Note
I’d be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).

Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!

Source: Dr. Greger –

Killing cancer like the common cold

Nick Wilkins was diagnosed with leukemia when he was 4 years old, and when the cancer kept bouncing back, impervious to all the different treatments the doctors tried, his father sat him down for a talk.

Cure of Leukaemia

John Wilkins explained to Nick, who was by then 14, that doctors had tried chemotherapy, radiation, even a bone marrow transplant from his sister.

“I explained to him that we’re running out of options,” Wilkins remembers telling his son.

There was one possible treatment they could try: an experimental therapy at the University of Pennsylvania.

He asked his son if he understood what it would mean if this treatment didn’t work.

Read More Here on

Curcumin and Knee Osteoarthritis

Curcumin and Knee  Osteoarthritis
One  hundred and seven patients with primary osteoarthritis of the knee were  studied, including those with knee pain on a scale of 5 to 10 in intensity;  radiographic osteophytes; and at least one of the following features: age  >50, morning stiffness <30 minutes in duration, and crepitus on motion.  The majority of the individuals were overweight women with a BMI >25.  Participants were asked to discontinue their knee pain medications and were  randomized to either ibuprofen 400 mg twice daily or Curcuma domestica extract,  500 mg four times daily for 6 weeks. Continue reading

Inhalation of Auto Emissions Turns HDL Cholesterol from ‘Good’ to ‘Bad’

Researchers have found in a study done on mice that breathing motor vehicle emissions triggers a change in high-density lipoprotein (HDL) cholesterol, altering its cardiovascular protective qualities so that it actually contributes t o clogged arteries.

 Inhalation of Auto Emissions Turns HDL Cholesterol from 'Good' to 'Bad': Researchers
In addition to changing HDL from “good” to “bad,” the inhalation of emissions activates other components of oxidation, the early cell and tissue damage that causes inflammation, leading to hardening of the arteries, according to the research team, which included scientists from UCLA and other institutions.

Continue reading

White blood cell enzyme contributes to inflammation and obesity

Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced -- neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low. (Credit: Sanford-Burnham Medical Research Institute)

Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced — neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low. (Credit: Sanford-Burnham Medical Research Institute)

Apr. 2, 2013 — Many recent studies have suggested
that obesity is associated with chronic inflammation in fat tissues. Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) have discovered that an imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. This enzyme is produced by white blood cells called neutrophils, which play an important role in the body’s immune defense against bacteria. The researchers found that obese humans and mice have increased neutrophil elastase activity and decreased levels of α1-antitrypsin, a protein that inhibits the elastase. When the team reversed this imbalance in a mouse model and fed them a high-fat diet, the mice were resistant to body weight gain, insulin resistance (a precursor to type 2 diabetes), and fatty liver disease. Their study appears April 2 inCell Metabolism.

What happens when you reduce neutrophil elastase levels
“The imbalance between neutrophil elastase and its inhibitor, α1-antitrypsin, is likely an important contributing factor in the development of obesity, inflammation, and other health problems. Shifting this balance — by either reducing one or increasing the other — could provide a new therapeutic approach to preventing and treating obesity and several obesity-related conditions,” said Zhen Jiang, Ph.D., assistant professor in Sanford-Burnham’s Diabetes and Obesity Research Center at Lake Nona, Orlando and senior author of the study.

This study began when Jiang and his team noticed that neutrophil elastase levels are particularly high and α1-antitrypsin levels are low in a mouse model of obesity. Then they saw the same thing in blood samples from human male volunteers.

To further probe this curious neutrophil elastase-obesity relationship, the researcher turned once again to mouse models. They found that mice completely lacking the neutrophil elastase enzyme don’t get as fat as normal mice, even when fed a high-fat diet. Those mice were also protected against inflammation, insulin resistance, and fatty liver. The same was true in a mouse model genetically modified to produce human α1-antitrypsin, which inhibits neutrophil elastase.

Normal mice on a high-fat diet were also protected against inflammation, insulin resistance, and fatty liver when they were given a chemical compound that inhibits neutrophil elastase. This finding helps validate the team’s conclusions about neutrophil elastase’s role in inflammation and metabolism and also suggests that a medicinal drug could someday be developed to target this enzyme.

Mechanism: how neutrophil elastase influences inflammation and metabolism

How do high neutrophil elastase levels increase inflammation and cause weight gain and other metabolic problems?

Jiang and his team began connecting the mechanistic dots. They discovered that neutrophil elastase-deficient mice have increased levels of several factors, including adiponectin, AMPK, and fatty acid oxidation. These are known for their roles in increasing energy expenditure, thus helping the body burn excess fat.

Journal Reference:

  1. Virginie Mansuy-Aubert, Qiong L. Zhou, Xiangyang Xie, Zhenwei Gong, Jun-Yuan Huang, Abdul R. Khan, Gregory Aubert, Karla Candelaria, Shantele Thomas, Dong-Ju Shin, Sarah Booth, Shahid M. Baig, Ahmed Bilal, Daehee Hwang, Hui Zhang, Robin Lovell-Badge, Steven R. Smith, Fazli R. Awan, Zhen Y. Jiang. Imbalance between Neutrophil Elastase and its Inhibitor α1-Antitrypsin in Obesity Alters Insulin Sensitivity, Inflammation, and Energy ExpenditureCell Metabolism, 2013; 17 (4): 534 DOI:10.1016/j.cmet.2013.03.005