Science Alert | There’s Something You Really Need to Know About IV Vitamin ‘Shots’



Want to boost your immune system, reduce your physical signs of ageing, or cleanse your blood to get rid of toxins? Intravenous (IV) vitamin therapy, or vitamin drips, promise to help.

Some claim they can even benefit serious conditions like cancer, Parkinson’s disease, the eye condition macular degeneration, the pain of fibromyalgia and depression.

Celebrities have promoted them on social media. The demand has led to alternative therapy lounges popping up around the world, including in Australia. Patients can kick back in comfy leather chairs while they’re hooked up to IVs in the infusion lounge, watch Netflix and have some tea.

But do they work? Or are you just paying for really expensive urine? Let’s look at what the science says.

What is IV vitamin therapy?

IV vitamin therapy administers vitamins and minerals directly into the bloodstream via a needle that goes directly into your vein. Fans of the therapy believe this enables you to obtain more nutrients as you avoid the digestion process.

Providers of these injections say they customise the formula of vitamins and minerals depending on the perceived needs of the patient.

Right now for example, many Australian lounges are offering drip “cocktails” containing immune boosting vitamins like vitamin C and zinc to help protect against the flu. Other popular therapy sessions come under names like “Energy Cocktail” and “Glow”. One vitamin IV therapy session can take 30-90 minutes and will cost between AU$80 to $1,000 (US$55 to $700).

Does IV vitamin therapy work?

IV therapy itself is not new and has been used in the medical profession for decades. In hospitals, it is commonly used to hydrate patients and administer essential nutrients if there is an issue with gut absorption, or long-term difficulty eating or drinking due to surgery.

Single nutrient deficiencies like vitamin B12 or iron are also often treated in hospital with infusions under medical supervision.

But the “cocktails” IV vitamin therapy clinics create and administer are not supported by scientific evidence. There have been no clinical studies to show vitamin injections of this type offer any health benefit or are necessary for good health.

In fact, there are very few studies that have looked at their effectiveness at all.

There is one review on the use of the “Myers’ cocktail” (a solution of magnesium, calcium, vitamin C and a number of B vitamins). But it just contains a collection of anecdotal evidence from singular case studies.

Another trial looked into the effectiveness of IV vitamin therapy in reducing symptoms of 34 people with the the chronic pain condition fibromyalgia. It found no significant differences between those who received the “Myers’ cocktail” once a week for eight weeks and those who did not.

In fact, the authors noted a strong placebo effect. In other words, many people said their symptoms improved when they were only injected with a “dummy” cocktail.

Another study that examined IV vitamin use in fibromyalgia patients was missing a placebo group, involved just seven patients and showed only short-term improvement in symptoms. The only other published study examined IV vitamin therapy use for asthma. But that study was of even poorer quality.

What are the risks of IV vitamin therapy?

Even when it comes to vitamins and minerals, you can have too much of a good thing. For example, if you take in more of the fat soluble vitamin A than you need, your body stores it, risking damage to major organs, like the liver.

IV vitamin therapy “cocktails” also often contain significant levels of the water soluble vitamins C and B. These are processed by the kidneys and excreted into urine when the body cannot store any more. This makes for some very expensive urine.

There is also the risk of infection with IV vitamin therapy. Any time you have an IV line inserted, it creates a direct path into your bloodstream and bypasses your skin’s defence mechanism against bacteria.

People with certain conditions like kidney disease or renal failure shouldn’t have IV vitamin therapy because they cannot quickly remove certain minerals from the body. For these people, adding too much potassium could lead to a heart attack.

People with heart, kidney or blood pressure conditions should also avoid IV vitamin therapy as there is risk of fluid overload without consistent monitoring. The consequences of fluid overload in these patients can include heart failure, delayed wound healing, and impaired bowel function.

What’s the bottom line?

For most of us, the quantities of vitamins and minerals needed for good health can be obtained by eating a healthy diet with a wide range of foods and food groups. Obtaining vitamins and minerals from your diet is much easier, cheaper, and safer.

Unless you have a medically diagnosed reason for getting a vitamin infusion and it was prescribed by your doctor, you are always better off obtaining vitamins and minerals through food. The ConversationTo read out more, please visit:

Emily Burch, Accredited Dietitian/Nutritionist & PhD Candidate, Griffith University.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Press Release | Autophagy and Mitochondria: Targets in Neurodegenerative Disorders (image)


Autophagy is a cellular degradation process that can cause the death of a cell in certain conditions. Autophagy is necessary to maintain cellular homeostasis by clearing out damaged cellular organelles and proteins through certain pathways. Mitochondria are cell organelles responsible for the constant supply of energy to maintain cellular physiology and energy metabolism.

Ashutosh Kumar et al. at the National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, India present a review on autophagy in neuronal cells. The researchers believe that autophagy on the neuronal cells can lead to neurodegenerative diseases and countering the effects of this process through targeted drugs can be beneficial in the fight against such diseases. Neuronal cells are more vulnerable to such bioenergetic depletion as most of their function crucially depends on availability of energy derived mainly from mitochondrial function. Any incidence of mitochondrial dysfunction inevitably results in neurodegeneration. Therefore, mitochondrial autophagy (mitophagy) plays an integral role in the onset of neurodegenerative diseases as the instance and failure of these pathways can have destructive effects on cellular homeostasis.

Previous studies show significant association between neurodegenerative disorders and mitochondrial dysfunction and abnormal mitophagy. Abnormal mitophagy leads to the accumulation of protein aggregates and consequential neurodegeneration. Future treatments for neurodegenerative disorders could involve drugs targeting mitochondria and autophagy-related proteins and enzymes. This review discusses the involvement of mitochondrial and autophagy dysfunction in neurodegenerative disorders specifically focusing on Alzheimer’s, Parkinson’s, and Huntington’s disease. Read full press release to find out more at:




This article by Dr. Ashutosh Kumar et al. is published in CNS & Neurological Disorders – Drug Targets, Volume 17, Issue 9, 2018. The article is Open Access till 31st January, 2019. To obtain the article, please visit:

EDITOR’S CHOICE ARTICLE | Models of Parkinson’s Disease with Special Emphasis on Drosophila melanogaster

Author(s): Ambreen Fatima, Smita Jyoti, Yasir Hasan Siddique*.

Graphical Abstract:


Background & Objective: Parkinson’s disease is the second most common neurodegenerative disorder affecting more than 1% of the population averaged 60 years of age. The majority of PD cases are sporadic and are probably caused by a combination of risk factors but 5-10% of the PD cases are familial. Due to the high degree of the gene, conservation in humans, mice and insects using an animal model system is a valuable approach to further elucidate the roles of the genes in PD.


Conclusion: The present review highlights the models used to study PD symptoms with special emphasis on Drosophila.



Browse the article details at:

EDITORS CHOICE ARTICLE – Dimerization of C-terminal Truncations of α-synuclein and its Effect on the Aggregation Propensity: A Potential of Mean Force Study

Journal Name: Current Chemical Biology

Author(s): Airy Sanjeev, Venkata Satish Kumar Mattaparthi*.






Graphical Abstract:



Background: The occurrence of Parkinson’s Disease (PD) is associated with the deposition of proteinaceous aggregates formed by the self-assembly of α-synuclein protein. The pathogenesis of PD has been reported to be linked with the α-synuclein gene. However, the presence of missense mutations: A30P, A53T, E46K, H50Q, G51D and A53E has also been linked with the autosomal inheritance of PD. Recently, it has been highlighted that C-terminal truncated α-synucleins undergo aggregation at a faster rate while the full-length α-synucleins are critical.

Objective: To study the dimerization of C-terminal truncations of α-synuclein and its effect on the aggregation propensity.

Methodology: We investigated the dimerization of the two important C-terminal truncations (120 and 123) of α-synuclein using Molecular Dynamics Simulation and Potential of Mean Force (PMF) study.

Results: From our PMF study, we observed that the binding free energy value to be larger for the association of C-terminal truncated α-synucleins than the value that has been reported for Wild-Type (WT) in our earlier study.

Conclusion: Truncating the C-terminal region (which is considered to be intra-molecular chaperone) in α-synucleins exposes the hydrophobic region and thereby increases the aggregation propensity.


EDITOR’S CHOICE – N-3 (Omega-3) Fatty Acids: Effects on Brain Dopamine Systems and Potential Role in the Etiology and Treatment of Neuropsychiatric Disorders

Journal: CNS & Neurological Disorders – Drug Targets

Author(s): Michelle Healy-Stoffel, Beth Levant

Graphical Abstract:



Background & Objective: A number of neuropsychiatric disorders, including Parkinson’s disease, schizophrenia, attention deficit hyperactivity disorder, and, to some extent, depression, involve dysregulation of the brain dopamine systems. The etiology of these diseases is multifactorial, involving genetic and environmental factors. Evidence suggests that inadequate levels of n-3 (omega- 3) polyunsaturated fatty acids (PUFA) in the brain may represent a risk factor for these disorders. These fatty acids, which are derived from the diet, are a major component of neuronal membranes and are of particular importance in brain development and function. Low levels of n-3 PUFAs in the brain affect the brain dopamine systems and, when combined with appropriate genetic and other factors, increase the risk of developing these disorders and/or the severity of the disease. This article reviews the neurobiology of n-3 PUFAs and their effects on dopaminergic function.

Conclusion: Clinical studies supporting their role in the etiologies of diseases involving the brain dopamine systems and the potential of n-3 PUFAs in the treatment of these disorders are discussed.

Read more here:

MOST ACCESSED ARTICLE – Therapeutic, Molecular and Computational Aspects of Novel Monoamine Oxidase (MAO) Inhibitors – Combinatorial Chemistry & High Throughput Screening

Journal: Combinatorial Chemistry & High Throughput Screening

Author(s): Muthusamy Ramesh , Yussif M. Dokurugu, Michael D. Thompson, Mahmoud E. Soliman


Background: Due to the limited number of MAO inhibitors in the clinics, several research efforts are aimed at the discovery of novel MAO inhibitors. At present, a high specificity and a reversible mode of inhibition of MAO-A/B are cited as desirable traits in drug discovery process. This will help to reduce the probability of causing target disruption and may increase the duration of action of drug.

Aim: Most of the existing MAO inhibitors lead to side effects due to the lack of affinity and selectivity. Therefore, there is an urgent need to design novel, potent, reversible and selective inhibitors for MAO-A/B. Selective inhibition of MAO-A results in the elevated level of serotonin and noradrenaline. Hence, MAO-A inhibitors can be used for improving the symptoms of depression. The selective MAO-B inhibitors are used with L-DOPA and/or dopamine agonists in the symptomatic treatment of Parkinson’s disease. The present study was aimed to describe the recently developed hits of MAO inhibitors.

Method: At present, CADD techniques are gaining an attention in rationale drug discovery of MAO inhibitors, and several research groups employed CADD approaches on various chemical scaffolds to identify novel MAO inhibitors. These computational techniques assisted in the development of lead molecules with improved pharmacodynamics / pharmacokinetic properties toward MAOs. Further, CADD techniques provided a better understanding of structural aspects of molecular targets and lead molecules.

Conclusions: The present review describes the importance of structural features of potential chemical scaffolds as well as the role of computational approaches like ligand docking, molecular dynamics, QSAR and pharmacophore modeling in the development of novel MAO inhibitors.

To access the article, please visit:


OPEN ACCESS ARTICLE – Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer – Current Neurovascular Research

Journal: Current Neurovascular Research

Author(s):  Kenneth Maiese


Background: The mammalian circadian clock and its associated clock genes are increasingly been recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease.

Methods: In light of the significant role circadian rhythm can hold over the body’s normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis.

Results: In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer’s disease and Parkinson’s disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth.

Conclusion: Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.

Read more here:

OPEN ACCESS ARTICLE – Comparative Neurophysiologic Study of Pain in Patients with Parkinson’s Disease and Patients with Persistent Pain After Spinal Surgery – Neuroscience and Biomedical Engineering

Journal: Neuroscience and Biomedical Engineering

Author(s): Masanaka Takeda, Hisao Tachibana, Fumiaki Okada, Shuhei Kasama, Hiroo Yoshikawa

Graphical Abstract:


Background: Pain is a common and troublesome non-motor symptom in Parkinson’s disease (PD). Similarly, severe postoperative pain is common after major spinal surgery and may become chronic. The pathophysiologic mechanism underlying those conditions remains unclear. In this study, we recorded pain-related evoked potentials induced by intra-epidermal electrical stimulation in patients with PD and patients with persistent pain after spinal surgery and compared the results between the two groups.

Objective: The purpose of this study was to investigate the pathophysiology of pain in patients with persistent pain after spinal surgery and in patients with PD.

Methods: We recorded pain-related evoked potentials in 23 patients with PD (64.0 years), 6 patients with persistent pain after spinal surgery (69.5 years) and 12 healthy controls (59.6 years).

Results: Major negative (N1) and positive (P1) deflections were observed after each stimulation. The amplitudes between N1 and P1 (N1-P1), which are thought to originate from the anterior cingulate cortex and insula, were significantly lower in both patients with PD and persistent pain after spinal surgery than in the controls (both P<0.01). However, there was no significant difference in N1-P1 amplitude between the patients with PD and the patients with persistent pain after spinal surgery. No significant differences in N1 and P1 latencies were observed among the three groups.

Conclusion: These results suggest that abnormal central processing of pain is present in patients with PD and those with chronic persistent pain after spinal surgery and that these two conditions share similar pathophysiologic mechanisms, at least partially.

Read more here:

Testimonial by Tamara Lazarević-Pašti!

Tamara Lazarevi-Pašti

Contributed Article: “Modulators of Acetylcholinesterase Activity: from Alzheimer’s Disease to Anti-cancer Drugs

Podcast: Targeting Human Astrocytes’ Calcium-sensing Receptors for Treatment of Alzheimer’s Disease

Author(s): Ikuko Miyazaki, Masato Asanuma.

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