Anti-inflammatory properties of short fasts (ADF, IF)

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Some members report gains from long term fasting (20-30 days). However there are not much studies on prolonged fasting. Intermittent fasting and Alternate Day Fasting are under intensive investigation in the last decade. I have some studies in my favorites. Results in men are somewhat controversial. In mice and rats however the results are very promising. Mice that go through ADF live 40% longer than ad libitum fed ones, and they live in better health. Many things are interesting about short term fasting: two that I remember are that Growth Hormone increase by about 20x in men during fasting and apparently (in mice at least i think), two neuromessaging peptides are activated to boost neurogenesis.

It is now some time that I have a beginning of phimosis (I am pretty sure finasteride did this). I tried treating with boric acid but results are not stable. Some days ago, I avoided dinner and breakfast. To my surprise the inflammation of most of the inflamed skin subsided for some days to an extent that boric acid did’t achieve. My penis was looking much normal. Also I can tell my erections improved somewhat. In this thread I would like to discuss and bring together, with your help possibly, some studies on
1-ADF, IF in general
2-Their anti-inflmmatory properties
3-The inflammatory nature of PFS
4-whatever you want related to this

For the second point there is much discussion on the fact that intermittent fasting appears to be damn anti-inflammatory. There is some material to read about this. For instance there is a study where 10 day fasting induced long lasting beneficial effects on rheumatoid arthritis.

About the 3rd point I would like to ask to the more experienced members in particular, if there is the feeling that inflammation might be an obstacle to healing. I have many conditions that can be related to inflammation, like penis pain, tingling in the scrotum, starting phimosis etc. To my opinion the most interesting theory is the one about the pudendal neuropathy when talking about sexual sides (this theory/fact apparently fits with the findings on AR and neurosteroids).

I will fast pretty soon on occasions, short (one/two meal) fasts because I have heart problems (thanks fin). I will let you know what happens to me if I don’t die. Please post your findings if you’re interested.

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Intermittent fasting during Ramadan attenuates proinflammatory cytokines and immune cells in healthy subjects. (Dec 2012)

Intermittent fasting and caloric restriction have been shown to extend life expectancy and reduce inflammation and cancer promotion in animal models. It was hypothesized that intermittent prolonged fasting practiced during the month of Ramadan (RIF) could positively affect the inflammatory state. To investigate this hypothesis, a cross-sectional study was designed to investigate the impact of RIF on selected inflammatory cytokines and immune biomarkers in healthy subjects. Fifty (21 men and 29 women) healthy volunteers who practiced Ramadan fasting were recruited for the investigation of circulating proinflammatory cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor α), immune cells (total leukocytes, monocytes, granulocytes, and lymphocytes), and anthropometric and dietary assessments. The investigations were conducted 1 week before Ramadan fasting, at the end of the third week of Ramadan, and 1 month after the cessation of Ramadan month. The proinflammatory cytokines IL-1β, IL-6, and tumor necrosis factor α; systolic and diastolic blood pressures; body weight; and body fat percentage were significantly lower (P < .05) during Ramadan as compared with before Ramadan or after the cessation of Ramadan fasting. Immune cells significantly decreased during Ramadan but still remained within the reference ranges. These results indicate that RIF attenuates inflammatory status of the body by suppressing proinflammatory cytokine expression and decreasing body fat and circulating levels of leukocytes.

ncbi.nlm.nih.gov/pubmed/23244540

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Wikipedia on autophagy:

Autophagy (or autophagocytosis) is the basic catabolic mechanism that involves cell degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery

Short-term fasting induces profound neuronal autophagy. (2010)

Disruption of autophagy–a key homeostatic process in which cytosolic components are degraded and recycled through lysosomes–can cause neurodegeneration in tissue culture and in vivo. Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy. One well-recognized way of inducing autophagy is by food restriction, which upregulates autophagy in many organs including the liver; but current dogma holds that the brain escapes this effect, perhaps because it is a metabolically privileged site. Here, we have re-evaluated this tenet using a novel approach that allows us to detect, enumerate and characterize autophagosomes in vivo. We first validate the approach by showing that it allows the identification and characterization of autophagosomes in the livers of food-restricted mice. We use the method to identify constitutive autophagosomes in cortical neurons and Purkinje cells, and we show that short-term fasting leads to a dramatic upregulation in neuronal autophagy. The increased neuronal autophagy is revealed by changes in autophagosome abundance and characteristics, and by diminished neuronal mTOR activity in vivo, demonstrated by a reduction in levels of phosphorylated S6 ribosomal protein in Purkinje cells. The increased abundance of autophagosomes in Purkinje cells was confirmed using transmission electron microscopy. Our data lead us to speculate that sporadic fasting might represent a simple, safe and inexpensive means to promote this potentially therapeutic neuronal response.

ncbi.nlm.nih.gov/pubmed/20534972

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I think there is something interesting behind this one

Dietary restriction supports peripheral nerve health by enhancing endogenous protein quality control mechanisms. (Dec 2012)

The peripheral nervous system (PNS) comprises of an extensive network of connections that convey information between the central nervous system (CNS) and peripheral organs. Long myelinated nerve fibers are particularly susceptible to age-related changes, as maintenance of the insulating glial membrane requires extensive synthesis and processing of many proteins. In rodent models, peripheral demyelination caused by genetic risk factors or by normal aging are attenuated by intermittent fasting (IF) or calorie restriction (CR) supporting a role for dietary intervention in preserving neural function. This review will summarize recent studies examining mechanisms by which life-long CR or extended IF supports peripheral nerve health.

ncbi.nlm.nih.gov/pubmed/23267845

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Dietary restriction started after spinal cord injury improves functional recovery. (Sep 2008)

Spinal cord injury typically results in limited functional recovery. Here we investigated whether therapeutic dietary restriction, a multi-faceted, safe, and clinically-feasible treatment, can improve outcome from cervical spinal cord injury. The well-established notion that dietary restriction increases longevity has kindled interest in its potential benefits in injury and disease. When followed for several months prior to insult, prophylactic dietary restriction triggers multiple molecular responses and improves outcome in animal models of stroke and myocardial infarction. However, the efficacy of the clinically-relevant treatment of post-injury dietary restriction is unknown. Here we report that “every-other-day fasting” (EODF), a form of dietary restriction, implemented after rat cervical spinal cord injury was neuroprotective, promoted plasticity, and improved behavioral recovery. Without causing weight loss, EODF improved gait-pattern, forelimb function during ladder-crossing, and vertical exploration. In agreement, EODF preserved neuronal integrity, dramatically reduced lesion volume by >50%, and increased sprouting of corticospinal axons. As expected, blood beta-hydroxybutyrate levels, a ketone known to be neuroprotective, were increased by 2-3 fold on the fasting days. In addition, we found increased ratios of full-length to truncated trkB (receptor for brain-derived neurotrophic factor) in the spinal cord by 2-6 folds at both 5 days (lesion site) and 3 weeks after injury (caudal to lesion site) which may further enhance neuroprotection and plasticity. Because EODF is a safe, non-invasive, and low-cost treatment, it could be readily translated into the clinical setting of spinal cord injury and possibly other insults.

ncbi.nlm.nih.gov/pubmed/18585708

Intermittent fasting improves functional recovery after rat thoracic contusion spinal cord injury. (2011 Mar)

Spinal cord injury (SCI) often results in a loss of motor and sensory function. Currently there are no validated effective clinical treatments. Previously we found in rats that dietary restriction, in the form of every-other-day fasting (EODF), started prior to (pre-EODF), or after (post-EODF) an incomplete cervical SCI was neuroprotective, increased plasticity, and promoted motor recovery. Here we examined if EODF initiated prior to, or after, a T10 thoracic contusion injury would similarly lead to enhanced functional recovery compared to ad libitum feeding. Additionally, we tested if a group fed every day (pair-fed), but with the same degree of restriction as the EODF animals (∼25% calorie restricted), would also promote functional recovery, to examine if EODF’s effect is due to overall calorie restriction, or is specific to alternating sequences of 24-h fasts and ad libitum eating periods. Behaviorally, both pre- and post-EODF groups exhibited better functional recovery in the regularity indexed BBB ambulatory assessment, along with several parameters of their walking pattern measured with the CatWalk device, compared to both the ad-libitium-fed group as well as the pair-fed group. Several histological parameters (intensity and symmetry of serotonin immunostaining caudal to the injury and gray matter sparing) correlated with functional outcome; however, no group differences were observed. Thus besides the beneficial effects of EODF after a partial cervical SCI, we now report that alternating periods of fasting (but not pair-fed) also promotes improved hindlimb locomotion after thoracic spinal cord contusion, demonstrating its robust effect in two different injury models.

ncbi.nlm.nih.gov/pubmed/21219083

Intermittent fasting in mice does not improve hindlimb motor performance after spinal cord injury. (2011 Jun)

Previously, we reported that every-other-day-fasting (EODF) in Sprague-Dawley rats initiated after cervical spinal cord injury (SCI) effectively promoted functional recovery, reduced lesion size, and enhanced sprouting of the corticospinal tract. More recently, we also showed improved behavioral recovery with EODF after a moderate thoracic contusion injury in rats. In order to make use of transgenic mouse models to study molecular mechanisms of EODF, we tested here whether this intermittent fasting regimen was also beneficial in mice after SCI. Starting after SCI, C57BL/6 mice were fed a standard rodent chow diet either with unrestricted access or feeding every other day. Over a 14-week post-injury period, we assessed hindlimb locomotor function with the Basso Mouse Scale (BMS) open-field test and horizontal ladder, and the spinal cords were evaluated histologically to measure white and grey matter sparing. EODF resulted in an overall caloric restriction of 20% compared to animals fed ad libitum (AL). The EODF-treated animals exhibited a ∼ 14% reduction in body weight compared to AL mice, and never recovered to their pre-operative body weight. In contrast to rats on an intermittent fasting regimen, mice exhibited no increase in blood ketone bodies by the end of the second, third, and fourth day of fasting. EODF had no beneficial effect on tissue sparing and failed to improve behavioral recovery of hindlimb function. Hence this observation stands in stark contrast to our earlier observations in Sprague-Dawley rats. This is likely due to the difference in the metabolic response to intermittent fasting as evidenced by different ketone levels during the first week of the EODF regimen.

ncbi.nlm.nih.gov/pubmed/21410319

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Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake

Dietary restriction has been shown to have several health benefits including increased insulin sensitivity, stress resistance, reduced morbidity, and increased life span. The mechanism remains unknown, but the need for a long-term reduction in caloric intake to achieve these benefits has been assumed. We report that when C57BL/6 mice are maintained on an intermittent fasting (alternate-day fasting) dietary-restriction regimen their overall food intake is not decreased and their body weight is maintained. Nevertheless, intermittent fasting resulted in beneficial effects that met or exceeded those of caloric restriction including reduced serum glucose and insulin levels and increased resistance of neurons in the brain to excitotoxic stress. Intermittent fasting therefore has beneficial effects on glucose regulation and neuronal resistance to injury in these mice that are independent of caloric intake.

pnas.org/content/100/10/6216.short

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Caloric restriction and intermittent fasting: Two potential diets for successful brain aging

The vulnerability of the nervous system to advancing age is all too often manifest in neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. In this review article we describe evidence suggesting that two dietary interventions, caloric restriction (CR) and intermittent fasting (IF), can prolong the health-span of the nervous system by impinging upon fundamental metabolic and cellular signaling pathways that regulate life-span. CR and IF affect energy and oxygen radical metabolism, and cellular stress response systems, in ways that protect neurons against genetic and environmental factors to which they would otherwise succumb during aging. There are multiple interactive pathways and molecular mechanisms by which CR and IF benefit neurons including those involving insulin-like signaling, FoxO transcription factors, sirtuins and peroxisome proliferator-activated receptors. These pathways stimulate the production of protein chaperones, neurotrophic factors and antioxidant enzymes, all of which help cells cope with stress and resist disease. A better understanding of the impact of CR and IF on the aging nervous system will likely lead to novel approaches for preventing and treating neurodegenerative disorders.

sciencedirect.com/science/ar … 3706000523

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Intermittent fasting alleviates the neuropathic phenotype in a mouse model of Charcot-Marie-Tooth disease

Charcot-Marie-Tooth type 1A (CMT1A) neuropathies linked to the misexpression of peripheral myelin protein 22 (PMP22) are progressive demyelinating disorders of the peripheral nervous system. In this study we asked whether dietary restriction by intermittent fasting (IF) could alleviate the neuropathic phenotype in the Trembler J (TrJ) mouse model of CMT1A. Our results show that neuropathic mice kept on a five month long IF regimen had improved locomotor performance compared to ad libitum (AL) fed littermates. The functional benefits of this dietary intervention are associated with an increased expression of myelin proteins combined with a thicker myelin sheath, less redundant basal lamina, and a reduction in aberrant Schwann cell proliferation. These morphological improvements are accompanied by a decrease in PMP22 protein aggregates, and enhanced expression of cytosolic chaperones and constituents of the autophagy-lysosomal pathway. These results indicate that dietary restriction is beneficial for peripheral nerve function in TrJ neuropathic mice, as it promotes the maintenance of locomotor performance.

(Free Article) ncbi.nlm.nih.gov/pmc/articles/PMC2757933/

[pax]

this is great stuff, tab, keep it coming

[tab]

Thanks, I think it is a viable way for promotion of recovery. It would take time probably, months at least. But stable improvements should arise. I’m already on it since two days. Strange days…I would say, maybe because of a headache.

Research in a variety of experiments shows that intermittent fasting is beneficial for the brain. Some of these findings come from animal experiments and still need to be replicated in humans. Still, natural experiments of people who engage in fasting for religious events (such as Ramadan) show that fasting is safe.

Some brain benefits of intermittent fasting include:

• resistance of brain cells to ischemic injury and stroke

• protection of neurons against genetic and environmental factors

• enhancement of synaptic plasticity

• protection against neurodegeneration

• increased production of BDNF

• reduction of neuronal damage

• protection against excitotoxicity

• protection against Alzheimer’s disease

• protection against Parkinson’s disease

• protection against Huntington’s disease

• maintenance of cognitive and motor performance

• enhancement of mitochondrial function

• enhancement of neuronal autophagy

References:
[Size=4]Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. (Link)
Caloric restriction and intermittent fasting: two potential diets for successful brain aging. (Link)
Caloric restriction increases learning consolidation and facilitates synaptic plasticity through mechanisms dependent on NR2B subunits of the NMDA receptor. (Link)
Calorie restriction and stroke. (Link)
Energy intake, meal frequency, and health: a neurobiological perspective. (Link)
Gene-diet interactions in brain aging and neurodegenerative disorders. (Link)
Interferon-gamma is up-regulated in the hippocampus in response to intermittent fasting and protects hippocampal neurons against excitotoxicity. (Link)
Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer’s disease. (Link)
Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. (Link)
Late-onset intermittent fasting dietary restriction as a potential intervention to retard age-associated brain function impairments in male rats. (Link)
Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms. (Link)
Molecular bases of caloric restriction regulation of neuronal synaptic plasticity. (Link)
Neuroprotective role of intermittent fasting in senescence-accelerated mice P8 (SAMP8) (Link)
Short-term fasting induces profound neuronal autophagy. (Link)[/size]

[spstriken]

undoubtedly fasting is the best medicine. But there are different kinds of fasting. I found stopping eating and drinking since morning to 6’O clock ( roughly 12 hour fast) is good although a bit difficult in the beginning. I am in contact to a former Accutane user who told me that he cured a lot through fasting. If any body interested, I can put his protocol here after taking his permission.

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I am indoubtly interested spstriken. I think that previous experiences are precious. I have set up a protocol for me but I am trying to improve it as I learn more on the subject. When I think it’s about complete I’ll post it too. I think that IF or similar fasts, are great for rehabilitation. However I think you cannot expect the fast to make miracles alone. There is psychiatric/psychological rehabilitation too to be done while on it; I think this way you can boost improvements. Very interesting on this front is that apparently IF increases brain plasticity, which I know is thought by someone to be one of the causes of pfs. Reduced neurosteroids indoubtly decrease neuronal plasticity.

I would say that a good meal at 12 am /1 pm is the ideal solution. I think you can even have a break at 10 am and eat something to avoid eating too much at 12am. In the morning you should have enough energies because of sleep. Then in the afternoon you have the energies because of the food. You should not loose the effects of the fast and by this way you avoid contraindications of excessive food intake in one meal.

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So far (1 week approx), no more prostate problems. Erection is not really good and I had shrinkage episodes. I believe this is due to the fact that whilst IF is good for health, it might have anxiety effects. I lost 1-2 kg probably because I also reduced the caloric intake. I feel a bit better mentally. Sperm apparently has increased in quantity. I don’t know if this is possible but my real gynecomastia apparently is getting less worse (this one would be really appreciated too). However glandular gynecomastia in itself is pretty variable in feeling. Fingers crossed.
There’s not much hunger in this method. I’m not suffering.

[esermon]

How long are you fasting per day? How many hours?

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So far I eat only in the evening, generally only one meal but I do not hesitate to eat outside that meal in the preceding or in the successive 2-3 hours. In general I would say I fast about 21-22 hours, the other 2-3 I eat, not continuously. I don’t take the count or I get crazy. I eat about everything, but I avoid junk food, alcohol (no I cannot withdraw nicotine) and I try to eat biologic when possible. I will have to switch eating at midday tomorrow.
I want to talk to my doctor; he will probably disagree of course, but I want to know what blood values I should monitor in order to avoid hurting myself. To all who want to try this way, please be careful with your health, honestly I am not really aware of the contraindications of this kind of fasting, and this is why I want to be careful, also because I want to be able to continue doing it. I started only because this was fascinating If you have some hints on this, you’re welcome.

PS I also walk 1 hour/day when possible. I don’t know if it is the case to go to the gym. I think walking is better at the beginning.

[kngreen60]

Ive started toying with fasting a bit too. Not 100% why, I just started. I dont think it will help my zero libido, but no reason not to try. So far just 12-16 hours 2-3 days a week. I was worried that it might hurt my usual 1+ hour of cardio, but so far I have more energy for this after work. We’ll see

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Let us know your progress, I’m very curious!
it’s been approx 2 weeks now since I started IF. As I said, what I noticed during this regimen was an increase amount of semen, not very much. Today I started a normal refeeding (well already yesterday I had some snacks), though all vegetables. At lunch I eat a vegetable soup(like grandma)and some fruits; and this evening, immediately after the dinner, the amount of semen was ENORMOUS compared to before the fast!!! I really didn’t expect that, maybe it’s from the soup I don’t know but I doubt it. I really hope this lasts, it’s the first time from the suspension of Fin that I see that amount. Will let you know if it lasts. I do not see spectacular improvements on the other sides but well who knows they might build up slowly. I feel more clear mentally, that’s what I am noticing somewhat.
The tingling on my pelvic floor, scrotum and penis was apparently getting worse during the fast. Today, maybe a bit better.
I am stopping the fast because I want to refeed my body since I do not usually eat a balanced diet, and this in conjunction with IF might denourish me. I’m also learning more on nutrition so I can possibly try to speed the IF improvements. I think I will go on a vegan-like diet, not completely but most of the time. This is also because I’m about to become hypertense and I want to smash the pressure down.

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This one’s a bit off topic and only if you end up with cancer but the sensitization effect on tissues might be interesting, whether it works also on androgen sensitivity.
Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy.

Short-term starvation (or fasting) protects normal cells, mice, and potentially humans from the harmful side effects of a variety of chemotherapy drugs. Here, we show that treatment with starvation conditions sensitized yeast cells (Saccharomyces cerevisiae) expressing the oncogene-like RAS2(val19) to oxidative stress and 15 of 17 mammalian cancer cell lines to chemotherapeutic agents. Cycles of starvation were as effective as chemotherapeutic agents in delaying progression of different tumors and increased the effectiveness of these drugs against melanoma, glioma, and breast cancer cells. In mouse models of neuroblastoma, fasting cycles plus chemotherapy drugs–but not either treatment alone–resulted in long-term cancer-free survival. In 4T1 breast cancer cells, short-term starvation resulted in increased phosphorylation of the stress-sensitizing Akt and S6 kinases, increased oxidative stress, caspase-3 cleavage, DNA damage, and apoptosis. These studies suggest that multiple cycles of fasting promote differential stress sensitization in a wide range of tumors and could potentially replace or augment the efficacy of certain chemotherapy drugs in the treatment of various cancers.

ncbi.nlm.nih.gov/pubmed/22323820

[Len]

i was curious … has anyone ever tried a “fermentation fast”? i do not know if this term actually exists, but what i basically mean is have nothing but water and kefir/ saurkraut etc. ? maybe a hard core dose of fermentation will have a really good effect on the gut flora and bring a little bit of relief?

i really feel these things help me a little bit, although i have never done JUST these things for a stretch

maybe i should try this just for a week or so and see what happens

the kefir will offer a little but of animal protein at the very least, i think, and the saurkraut is a vegetable

i may actually try this just to see if it makes me feel a little bit better

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I dont’ know Lennon, normally the greatest effects of fasting are gain when you only drink water. But who knows. You can look at this “full or near recovery stories” thread if you haven’t already

viewtopic.php?f=6&t=6142