Put on your thinking caps. It’s one of those posts.
1 in 100 people on average have or will develop schizophrenia. When I heard that statistic, I was shocked. I didn’t realize it was so common. Okay, so it’s only 1% of the population? Still. Go to a Lady Gaga concert. Now do the math. In my opinion, that’s too many people walking around in one venue with such a burdensome illness. The good news is that researchers are trying to figure out schizophrenia’s etiology and pathogenesis so that they can do something about it. That’s great news for the next few generations. It’s tough for people in the now who are so intimately acquainted with this disease.
The latest research has given us a few theories. One of these theories is the cytokine theory. If you have RA, then you’ll know what cytokines are. They are proteins, and they do many, many things in the body, but for the sake of this discussion I am going to discuss them in the context of the immune system. One thing that they are associated with is inflammation:
The pathogenesis of schizophrenia has yet to be fully characterized. Gene–environment interactions have been found to play a crucial role in the vulnerability to this disease. Among various environmental factors, inflammatory immune processes have been most clearly implicated in the etiology and pathology of schizophrenia. Cytokines, regulators of immune/ inflammatory reactions and brain development, emerge as part of a common pathway of genetic and environmental components of schizophrenia. Mater- nal infection, obstetric complications, neonatal hypoxia and brain injury all recruit cytokines to mediate inflammatory processes. Abnormal expres- sion levels of specific cytokines such as epidermal growth factor, interleukins (IL) and neuregulin-1 are found both in the brain and peripheral blood of patients with schizophrenia. Accordingly, cytokines have been proposed to transmit peripheral immune/ inflammatory signals to immature brain tissue through the developing blood–brain barrier, perturb- ing structural and phenotypic development of the brain. This cytokine hypothesis of schizophrenia is also supported by modeling experiments in animals. Animals treated with specific cytokines of epidermal growth factor, IL-1, IL-6, and neuregulin-1 as embryos or neonates exhibit schizophrenia-like behavioral abnormalities after puberty, some of which are ame- liorated by treatment with antipsychotics. In this review, we discuss the neurobiological mechanisms underlying schizophrenia and novel antipsychotic candidates based on the cytokine hypothesis. (online source)
This implies that schizophrenia is neurodevelopmental meaning that the disease’s etiology actually begins prenatally. The next question is: Does pro-inflammatory action continue postnatally and into and past the prodrome of the disease?
A January 2014 study published in Psychiatry Weekly suggests the affirmative:
Activation of inflammatory pathways is one among many hypotheses exploring the pathophysiology of schizophrenia. A number of studies suggest that prostaglandin E2 (PGE2), C-reactive protein, and proinflammatory cytokines are all increased in schizophrenia patients. Furthermore, schizophrenia patients who respond to treatment have shown lower inflammatory markers compared to treatment outset. The same is also seen in major depressive disorder, bipolar disorder, and regarding oxidative stress markers. “One may be led to believe that vulnerability to mental illness may somehow be related to neuroinflammation,” says Dr. Christoph Correll, “and therefore the question becomes: could symptoms be reduced by reducing inflammation?” (Psychiatry Weekly)
So, what do we do with this information? And, what about this mention of major depressive disorder and bipolar disorder? Neuroinflammation is possibly present there as well?
Let’s start here:
Here’s the abstract:
Turmeric (rich in curcuminoids) and ginger (rich in gingerols and shogaols) rhizomes have been widely used as dietary spices and to treat different diseases in Ayurveda/Chinese medicine since antiquity. Here, we compared the anti-inflammatory/anti-oxidant activity of these two plants in rat adjuvant-induced arthritis (AIA). Both plants (at dose 200 mg/kg body weight) significantly suppressed (but with different degrees) the incidence and severity of arthritis by increasing/decreasing the production of anti-inflammatory/pro-inflammatory cytokines, respectively, and activating the anti-oxidant defence system. The anti-arthritic activity of turmeric exceeded that of ginger and indomethacin (a non-steroidal anti-inflammatory drug), especially when the treatment started from the day of arthritis induction. The percentage of disease recovery was 4.6-8.3% and 10.2% more in turmeric compared with ginger and indomethacin (P < 0.05), respectively. The present study proves the anti-inflammatory/anti-oxidant activity of turmeric over ginger and indomethacin, which may have beneficial effects against rheumatoid arthritis onset/progression as shown in AIA rat model.
Here’s the thing about animal studies. If you want to know what’s going to be happening in medicine and pharmacology ten to twenty years from now, then you have to look at present animal studies. That’s where the cutting edge of medicine is because this is where researchers are asking the questions about modern diseases. What is the one thing that scientists keep running into when they talk about disease onset and progression? Inflammation. It is a marker for disease. Inflammation in the body is the immune system at work, and it’s been in the news for the last decade.
What is the important takeaway from one animal study about arthritis? Turmeric was more potent than indomethacin (NSAID) in treating rheumatoid arthritis onset and progression in animal models. Turmeric! A spice! This means that turmeric interacts with the body’s cytokines, and this is really important. My next question is: Does turmeric cross the blood/brain barrier?
Turmeric has been in use since ancient times as a condiment and due to its medicinal properties. Curcumin, the yellow colouring principle in turmeric, is polyphenolic and major active constituent. Besides anti-inflammatory, thrombolytic and anticarcinogenic activities, curcumin also possesses strong antioxidant property. In view of the novel combination of properties, neuroprotective efficacy of curcumin was studied in rat middle cerebral artery occlusion (MCAO) model. Rats were subjected to 2 h of focal ischemia followed by 72 h of reperfusion. They were pre-treated with curcumin (100 mg/kg, po) for 5 days prior to MCAO and for another 3 days after MCAO. The parameters studied were behavioural, biochemical and histological. Treatment with curcumin could significantly improve neurobehavioral performance compared to untreated ischemic rats as judged by its effect on rota-rod performance and grid walking. A significant inhibition in lipid peroxidation and an increase in superoxide dismutase (SOD) activity in corpus striatum and cerebral cortex was observed following treatment with curcumin in MCAO rats as compared to MCAO group. Intracellular calcium levels were decreased following treatment with curcumin in MCAO rats. Histologically, a reduction in the infarct area from 33% to 24% was observed in MCAO rats treated with curcumin. The study demonstrates the protective efficacy of curcumin in rat MCAO model. (Anti-ischemic effect of Curcumin on Rat Brain)
This study was addressing strokes; however, it proves one thing. Turmeric crosses the blood/brain barrier and acts as a neuroprotective agent. If that’s not enough, here’s one more article discussing turmeric’s action in the brain regarding Alzheimer’s Disease:
This paper discusses the effects of curcumin on patients with Alzheimer’s disease (AD). Curcumin (Turmeric), an ancient Indian herb used in curry powder, has been extensively studied in modern medicine and Indian systems of medicine for the treatment of various medical conditions, including cystic fibrosis, haemorrhoids, gastric ulcer, colon cancer, breast cancer, atherosclerosis, liver diseases and arthritis. It has been used in various types of treatments for dementia and traumatic brain injury. Curcumin also has a potential role in the prevention and treatment of AD. Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD. A growing body of evidence indicates that oxidative stress, free radicals, beta amyloid, cerebral deregulation caused by bio-metal toxicity and abnormal inflammatory reactions contribute to the key event in Alzheimer’s disease pathology. Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with AD has improved. This paper reviews the various mechanisms of actions of curcumin in AD and pathology. (The effects of curcumin (turmeric) on Alzheimer’s Disease: An overview)
If the cytokine theory or even the microglial theory is true and the etiology of schizophrenia is related to or even partially related to an immune response, then turmeric fits the bill as an adjunct treatment. It has a very low side-effect profile particularly when you compare it to lithium and antipsychotics. Turmeric is also a broad spectrum anti-viral. I have been taking it for two years, and I rarely get sick. I also rarely need to take ibuprofen since taking turmeric faithfully. It truly is as effective as an NSAID, when taken daily, for managing chronic pain.
For detailed information on turmeric, read this: Linus Pauling Institute Macronutrient Information Center
And wouldn’t you know it, someone recently finished a clinical trial using curcumin as an adjunct therapy in treatment for schizophrenia: Open-label study using Curcumin C-3 Complex in Schizophrenia. The results aren’t posted yet, but I’m dying to know what they are.