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Little evidence for SSRI use in anxiety and compulsions in ASD: my interview on Nourishing Hope for Autism Summit

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One of the reasons I’m so passionate about participating on summits like The Nourishing Hope for Autism Summit and sharing the powerful nutritional interventions is due to the fact that medications such as antidepressants and benzodiazepines are frequently prescribed in ASD – and the research and clinical evidence shows that children and adolescents with ASD (autism spectrum disorder) are more vulnerable to the side effects.

This paper, Psychopharmacological interventions in autism spectrum disorder, makes the following conclusion:

Psychopharmacological treatment of core and associated symptoms in ASD is challenging, in large part because ASD presents in many different ways. Furthermore, children and adolescents with ASD are more vulnerable to the side effects of psychopharmacological intervention than their age-matched, typically developing counterparts.

This paper, Pharmacotherapy of emotional and behavioral symptoms associated with autism spectrum disorder in children and adolescents, supports this, stating there is little evidence to support the use of SSRIs in ASD:

Selective serotonin reuptake inhibitors are often used in clinical practice to target anxiety and compulsions; however, there is little evidence to support its use in this population. There is a great need for further research on the safety and efficacy of existing psychotropic medications in youth with ASD.

And this paper published a few months ago, An update on pharmacotherapy of autism spectrum disorder in children and adolescents, concludes that

Overall, the evidence is limited for pharmacotherapy in children with ASD, and side-effects with long-term use can be burdensome.

Much of this also applies to adults with ASD and in my interview I talk about the psychiatric medicine concerns within the ASD community and the high incidence of anxiety, aggression, irritability and OCD in this population.

We also discuss the following nutritional solutions in my interview (appropriately titled: How to calm anxiety, and eliminate aggression and OCD) –

  • the role low serotonin plays in anxiety, aggression and OCD/obsessions and the use of tryptophan and when to avoid 5-HTP
  • the low GABA type of physical anxiety and how to effectively use GABA for results
  • how to use inositol for OCD and some wonderful success stories
  • lead toxicity and increased anxiety and the protective role of tryptophan and ascorbic acid
  • phenols and oxalates other special diets (and my story with oxalate issues)

Our interviews are always fun, science based and practical – and in this one we even shared some of our personal results (both good and bad) with some of these nutrients.

Here are just a few of the speakers and topics I’m really looking forward to hearing:

  • James Adams, PhD: The Scientific Evidence Linking Nutrition and Autism Improvement
  • Dietrich Klinghardt: Understanding Lyme, Infections, Mold, and Heavy Metals and the Effects on Autism
  • Chef Pete Evans: Food is Medicine, Inspiration from a chef
  • Kaalya Daniel, PhD: How You Can Use the Healing Properties of Camel’s Milk for Autism
  • Dominic D’Agostino, PhD: Is the Ketogenic Diet Right for an Autistic Child?
  • Susan Owens, MS: The Inflammasome, Oxalates, Autoimmunity and Autism
  • And of course, Julie Matthews, CNC: When GFCF Diets Don’t Work – BioIndividual Nutrition for Autism

This summit provides you with information and tools that address the root causes so medications such as the above do not even have to come into the picture!

The Nourishing Hope for Autism Summit runs July 30 to August 3 and is hosted by my dear friend and colleague Julie Matthews, whose work you’re probably very familiar with. In case Julie’s work is new to you, in my eyes, she is THE autism nutrition expert. I’ve had the pleasure of interviewing her a number of times on the Anxiety Summit, I endorse her Bioindividual Nutrition training (special diets) for practitioners, I highly respect the work she does and I adore her!

The focus of this summit is clearly autism and Julie is THE expert so you’ll learn a ton from the experts she has gathered.

But do keep in mind that those with autism or Asperger’s are often considered the canaries in the coalmine and even if you don’t have a loved one with ASD many of the interviews have wider applications for anxiety, ADHD and other developmental and learning disorders.

Register here for The Nourishing Hope for Autism Summit to learn more! It airs online from July 30 to August 3, 2018

Kate Spade: suicide, hormonal imbalance, antidepressants as a trigger and the stigma of mental health

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Photo by Paul Keleher (originally posted to Flickr as kate spade) [CC BY 2.0], via Wikimedia Commons
Kate Spade, a well-known American fashion icon and handbag designer, died by suicide last week at the age of 55. I’m always torn in situations like this…just share the news story with my sympathies in order to respect the family or use this as an opportunity to learn from and prevent others from suffering the same fate. This time I’m doing the latter – with the risk of appearing insensitive – because there are red flags here and I feel so strongly that we all need to learn from this in order to move mental health forward. I’m hoping her husband and family would approve.

In the announcement about Kate Spade’s suicide in the New York Times, Mr. Spade said:

that though his wife had suffered from anxiety at points during their relationship and marriage, her serious bouts of depression only began about six years ago, at the age of 49.

Kate suffered from depression and anxiety for many years. She was actively seeking help and working closely with her doctors to treat her disease, one that takes far too many lives. We were in touch with her the night before and she sounded happy. There was no indication and no warning that she would do this. It was a complete shock. And it clearly wasn’t her. There were personal demons she was battling.

My heart goes out to Kate Spade’s husband, young daughter and loved ones. Her suicide is just so sad but as I said I have a fair bit to say about this….

 

Hormone imbalance triggering anxiety and depression?

According to the reports, Kate’s “serious bouts of depression only began about six years ago, at the age of 49, but she had suffered “from depression and anxiety for many years”.

Perimenopause and menopause is a classic time for women to experience worsening anxiety and depression and can be driven by fluctuating hormones, especially low estrogen. In this study, Depression and the menopause: why antidepressants are not enough? the authors share that

Postmenopausal depression is more severe, has a more insidious course, is more resistant to conventional antidepressants in comparison with premenopausal women and has better outcomes when antidepressants are combined with HT (hormone therapy).

Addressing hormone imbalance as one possible root cause can eliminate the anxiety and depression. Some of my favorite resources for hormone balance are these books: The Hormone Secret and Cooking for Hormone Balance.

 

Low levels of neurotransmitters like serotonin, catecholamines and GABA?

Directly connected to hormonal imbalance is brain chemistry imbalance. Addressing low levels of neurotransmitters like serotonin, the catecholamines and GABA provide results quickly when they are used in a targeted way based on individual needs:

  • Low serotonin is an issue when estrogen levels are declining and the amino acid tryptophan can have profound benefits if low serotonin is one of the root causes, leading to depression, worry, fear, overwhelm and sleep issues.
  • Low catecholamines can cause the “I just want to say in bed” depression and low motivation, together with fatigue and poor focus. The amino acid tyrosine can help to eliminate some of this and also provides thyroid support.  Poor thyroid health can also be a root cause of depression.
  • We see low GABA levels when progesterone is low and if this is one of the root causes, it can result in increased physical anxiety and insomnia. The amino acid GABA, opened on to the tongue, can provide calming results within minutes.

I can totally relate to the hormonal aspect as I suffered from PMS for years and my anxiety issues and panic attacks started in my late 30s and I had a really low spell as I was going through menopause.  Both GABA and tryptophan turned things around very quickly for me as they do for my clients.

 

The role of diet and nutritional psychiatry?

There is so much new science behind the role of a real foods traditional diet for alleviating both depression and anxiety. The SMILES study, published by Prof Felice Jacka early 2017, was the first randomized controlled diet depression study and ONE THIRD of the dietary intervention group saw improvements in their depression symptoms.  This was just diet alone and switching from processed and junk food to real food with no specific dietary restrictions.

There is also much clinical evidence supporting how diet can have an impact. Holly, suffered from with severe depression and anxiety changed her diet and shared this with me:

Over the course of a year and a half, I was given 10 different psychiatric diagnoses and cycled through 10 different medications. I discovered the healing power of diet completely by accident, and it changed my life. I now live with no diagnoses and no symptoms.

I started with the Whole30 (strict paleo), then went paleo, dabbled with a ketogenic approach, and now I eat a modified paleo diet, with some rice and goat dairy.

This has been termed nutritional psychiatry and you can read more diet-depression and diet-anxiety success stories here.

Keep in mind that your prescribing psychiatrist may not yet be on board with this or up to date on the newest research. Just last week someone told me what happened when they discussed nutritional psychiatry with their doctor and showed them my book The Antianxiety Food Solution (my Amazon link). He said: “Good luck with that!”

 

Could the antidepressant medication have triggered her suicide?

The statement from Kate’s husband says “She was actively seeking help for depression and anxiety over the last 5 years, seeing a doctor on a regular basis and taking medication for both depression and anxiety.”  Could the antidepressant medication have triggered her suicide or played some part?

We will never know with Kate but this is always my first thought when I learn of a suicide and when we hear of homicides in the news. One of my colleagues shared this when her suicide was first announced: “I was wondering if she was under psych care and what role meds might have played in this tragedy.”

This paper is one of many papers reporting similar antidepressant suicide and violence risks, and concludes that:

Antidepressants double the occurrence of events in adult healthy volunteers that can lead to suicide and violence

Kelly Brogan MD – Holistic Psychiatrist​ no longer prescribes psychiatric medications because we don’t know who will experience this side-effect. She writes this about a Swedish study and antidepressants and increased suicides

As antidepressant prescriptions increased 270% over 15 years, suicide rates also increased. Strikingly, more than half of the young women who committed suicide (52%) were prescribed antidepressants within a year of committing suicide. And antidepressants were detected in 41% of the women who committed suicide, showing that they were under the influence of antidepressants at the time of death. 

 

What if you are taking an antidepressant and seeing benefits?

When I posted some of this on Facebook earlier in the week someone who is on an antidepressant and benefiting shared her frustration that we are blaming suicide on medications.

There are many who do benefit but there are two issues I have:

  1. Even if someone is doing well on an antidepressant, benzodiazepine or other psychiatric medication I feel we need informed consent about the side-effects and training for the individual and family on what to look out for as things can change. The can occur when meds are changed, doses are increased or decreased, new meds are added, one or more are stopped abruptly or too quickly (called discontinuation syndrome). Many doctors also need to be educated and to acknowledge that suicide and homicide are very real side-effects of these meds.
  2. We don’t know who will be adversely impacted, which is why consent/knowledge about this is so important.

When we rent ski equipment or go bungee jumping we sign an informed consent form, acknowledging the possible risks of death. Why is this not happening with these medications? I just want individuals to be going into this with eyes wide-open so they don’t say “why didn’t anyone tell us this?”

If someone is currently seeing benefits from antidepressants (or benzodiazepines) I make sure they know ALL the risks and encourage them to continue to look for root the causes and address these (never stopping medications abruptly and never without the prescribing doctor’s permission).

There are many possible biological or biomedical or metabolic causes of depression and anxiety and many of these can play a factor in suicide.  Here is a list of just some of them:

My concern is that none of these – the medications or poor diet and nutritional deficiencies – are ever discussed when someone does commit suicide or goes on a violent or homicidal rampage.

 

The stigma of mental health and the fear of seeking help

There are reports that “Kate Spade felt unable to seek help or discuss her mental health because she feared this might damage the brand she created.”  This is a huge issue and if it was true for her or if anyone with a mental health condition feels like this, this has to change!

As Dr. Mark Hyman MD​ said this when I interviewed him last year before the launch of his Broken Brain docu-series

I began to realize that the body was driving a lot of this brain dysfunction, and that if you fix the body, a lot of the brain disorders would get better, that it wasn’t a primarily a mental problem, but it was a physical problem.

Our interview and full transcript is here and we cover the gamut in 12 minutes: the gut and microbiome, nutritional deficiencies, food sensitivities, heavy metals, other environmental toxins and medications.

We don’t hide the fact that we have a broken leg so why do we have to hide it when we have a broken brain? If we can start to acknowledge that mental health issues so often have this physical aspect (and often it’s 100% physical) then hopefully we can end this crazy stigma.

And even if there is also trauma or lifestyle factors that make someone depressed or anxious – so be it. Stop the stigma and shame. Why do we have to put on a brave face and pretend all is well. It has to stop so people can ask for help.

Last but not least, I feel we need to offer practical nutritional psychiatry resources to the family who have been traumatized by the loss of a loved one to suicide.  We know the amino acids and B vitamins help individuals recover from psychological stress after a natural disaster and these same nutrients can help the family in the midst of their sorrow.

I am aware it’s a very delicate subject and I’m sure this will rub some people the wrong way but I believe we all need to be talking about this and not tip-toeing around it.

I really feel this all needed to be said today. I hope this helps you or a loved one.

Rest in peace Kate Spade.

Alzheimer’s disease: address the root cause to reverse symptoms (Microbiome summit)

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Dr. Jill Carnahan’s interview on the Microbiome Medicine Summit 2 covers cutting edge new information about Alzheimer’s disease, based on the work and research of Dr. Dale Bredesen. They start with the gut-brain connection and Dr. Carnahan shares this:

we used to think of early-onset cognitive decline and dementias and mood disorders as being in their own bucket. And so, we saw psychiatrists or neurological doctors or neurologists to treat those diseases. And now we’re finding as we knew for several years with functional medicine that, obviously, it’s all connected.

And the gut is especially important because this reservoir holds so many of our microbes and possibly pathogens and that speaks to the brain through the vagus nerve and through cytokines and through inflammatory molecules of all types.

And so, this conversation between our gut and our brain is very profound and has a huge impact on things like multiple sclerosis or dementia, Alzheimer’s, or even things like bipolar disorder, schizophrenia, depression, anxiety, and sleep disorders.

So what we’re finding is by addressing the immune system and the gut which are intricately connected, we can often get profound effects on areas in the body that are far from that, like the brain.

Dr. Kellman asks Dr. Carnahan to share a study that will be the slam dunk for really believing in this connection and she mentions a paper titled Microbes and Alzheimer’s Disease. It cites pathogens like herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete which can affect the brain and play a role in Alzheimer’s disease.

Dr. Carnahan then covers Dr. Dale Bredesen’s subtypes of early-onset dementia which allows you to treat the root cause and actually reverse symptoms. She goes into it in great detail so I’m going to give you the summary version here:

Type #1 is inflammatory

  • This could be from inflammation or infections or other poor dietary habits. And that’s where the microbiome could play into that.
  • You might see elevated CRP, IL-6, TNF-alpha. You might see a low albumin to globulin ratio. You might see high homocysteine, hypothyroid, elevated cortisol

Type #1.5 is glycotoxic

  • The pure pre-diabetic, diabetic
  • That’s kind of the pure elevated insulin, elevated fasting blood sugar, elevated cortisol, low testosterone, high triglycerides, low HDL (and has an element of inflammation)

Type #2 is atrophic: So that’s someone who loses their trophic factor of support like estrogen, testosterone, insulin, and vitamin D3.

And often, these type 1s and type 2s actually have ApoE-4 double mutations which are higher risk for Alzheimer’s.

Type #3 is toxic:

  • Toxic mold exposure, biotoxins from Lyme disease, or heavy metals or other chemicals.
  • Often these chemicals will act on the tight junctions of the gut and increase permeability. And then that permeability leads to massive endotoxemia.
  • Younger onset of symptoms (like 40s and 50s) and reversible once you find and remove the root cause

Type #4 is vascular: inflammation of the blood vessels, high homocysteine

Type #5 is traumatic: wrestlers or boxers or football players that have had multiple head injuries or trauma.

By addressing the various root causes, Dr. Bredesen reports a reduction and in some instances reversal of dementia symptoms.

Of course, we know anxiety is common when it comes to Alzheimer’s and dementia. By addressing many of these above root causes we’re also able to reduce anxiety symptoms at the same time.

It was a fascinating interview and I hope you enjoy it as much as I did. I learned a great deal and find it very useful to group the symptoms into types.

There does seem to be one aspect that Dr. Carnahan didn’t address and I haven’t seen it covered in Dr. Bredesen’s papers: the impact of benzodiazepines on dementia and Alzheimer’s disease.  There is conflicting research on this but I feel there is enough research that does show a correlation – enough for us to be concerned.   Here is a recent paper looking at high-dose benzodiazepine use in Chinese patients , supporting an association.

This 2016 paper – Benzodiazepine Use and Risk of Dementia in the Elderly Population: A Systematic Review and Meta-Analysis states:

Our results suggest that benzodiazepine use is significantly associated with dementia risk. However, observational studies cannot clarify whether the observed epidemiologic association is a causal effect or the result of some unmeasured confounding variable. Therefore, more research is needed.

This may likely fall under type #3 (toxic).  I plan to reach out to them as a follow-up.

UPDATE: May 9, 2017.  I did hear back from Dr. Carnahan and she shared that she always discusses history and physical and lab testing, and history of benzodiazepine use or other neuroactive substances. 

And new research shows that it’s more than the benzodiazepines: SSRIs, SRNIs and atypical antipsychotics increase the risk of dementia in veterans with PTSD and even in those who don’t have PTSD. 

I hope you’ll join the host Dr. Raphael Kellman and all the great speakers on the Microbiome Medicine Summit 2, May 8-15, 2017 to learn more.

If you have questions or comments please feel free to share in the comments.

 

Vulvodynia: oxalates, GABA, tryptophan and physical therapy

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On a recent webinar with Julie Matthews, I shared how healthy foods that are high in oxalates caused me excruciating foot pain: Oxalates and leaky gut for Anxiety.

We also mentioned how oxalates can be a factor in vulvodynia and someone asked this question on the blog:

I just listened to the webinar talking about oxalates. I was shocked and delighted to hear the mention of the connection between high oxalates and vulvodynia. My friend has suffered with this for 18 months with little improvement. She has painful feet so I am wondering if there is indeed a connection for her situation. Could you please explain a bit more of the vulvodynia/ oxalates connection? I would like to give my friend the information.

Before I share the resources I offered her for her friend, let me share this about vulvodynia:

Vulvodynia is defined as chronic vulvar burning, stinging, rawness, soreness or pain in the absence of objective clinical or laboratory findings to explain these symptoms. Vulvodynia is a chronic pain syndrome affecting up to 18% of the female population and is generally regarded as an underdiagnosed difficult to treat gynecological disorder.

There is still much we have to learn about vulvodynia and the causes are multifactorial:

The etiology [cause] of vulvodynia is still enigmatic and is probably multifactorial-including physiological concerns (eg, pelvic floor muscle dysfunction, neuropathic pain, and psychosocial) and sexual issues (eg, anxiety and sexual dysfunction). Although it is a common syndrome, most patients are neither correctly diagnosed nor treated. A diagnosis of vulvodynia is based upon patient history and lack of physical findings upon careful examination. No clinical or histological findings are present to aid in diagnosis. Most treatment options for vulvodynia are neither well studied nor have an evidence base, relying instead upon expert opinion, care provider experience, and use of data from other pain syndromes. However, many patients show marked improvement after physical therapy for the pelvic floor, medications for neuropathic pain, and psychosexual therapy.

You’ll notice that oxalates and other dietary approaches are not mentioned. There are actually 2 studies that state there is NO connection between dietary oxlalates and vulvodynia. This is the first one: Influence of dietary oxalates on the risk of adult-onset vulvodynia. The second paper: Urinary oxalate excretion and its role in vulvar pain syndrome concludes that:

Urinary oxalates may be nonspecific irritants that aggravate vulvodynia; however, the role of oxalates as instigators is doubtful.

In this paper: Vulvar vestibulitis-a complex clinical entity, a low oxalate diet and calcium citrate did help:

Successful outcomes were achieved in 14.3% of patients using a low oxalate diet and calcium citrate supplementation

The Vulval Pain Society is a wealth of information on vulvodynvia and they have this information on the low oxalate diet, saying it helps many women and it worth trying:

A diet low in oxalate salts has been suggested as a treatment for women who experience unexplained vulval pain or vulvodynia… it is widely used in the United States as a treatment for vulvodynia. The diet may be supplemented with the use of oral calcium citrate.

There are few doctors in the UK who are aware of or routinely use this treatment. Many specialist doctors who run vulval clinics in this country [the UK] are skeptical about the treatment, as much of the evidence has not been published in the medical literature and the treatment is not of proven value. A diet low in oxalate with or without calcium citrate may, however, benefit some women with vulval pain and this is certainly an option for some women to try.

The vulvar pain is often described as a “burning” or “cutting” or “sharp” kind of pain. You’ll see medications recommended for the neuropathic pain in many of the studies and on the Vulval Pain society site.

It does concern me that so many women are prescribed SSRIs and medications like gabapentin and benzodiazepines when there are the safer and more effective options of the amino acids such as tryptophan and GABA.   When dosed correctly these individual amino acids help with some of the pain and anxiety right away while other root causes are addressed. 

For my clients, I recommend targeted individual amino acids instead of the medications. I recommend a trial of tryptophan instead of an antidepressant, assuming they score low on the serotonin section of the amino acid questionnaire.

Research shows there is serotonin involvement with vulvodynia. In this study of women with PVD (provoked vestibulodynia i.e. pain in the entrance of the vagina, common with vulvodynia):

Polymorphism in the serotonin receptor gene, 5HT-2A, has been associated with other chronic pain disorders such as fibromyalgia…. The results [of this study] indicate a contribution of alterations in the serotonergic system to the patho-genesis of PVD and gives further evidence of PVD being a general pain disorder similar to other chronic pain disorders.

I also recommend a trial of GABA instead of gabapentin or one of the benzodiazepines, assuming they score low on the GABA section of the amino acid questionnaire.

Tryptophan and GABA can help with both the pain, and the anxiety and depression that is commonly seen with vulvodynia and other pelvic floor conditions – right away while other root causes are addressed.

Since acupuncture is often reported to be helpful, I also consider a trial of DPA for endorphin boosting and hence some pain reduction too.

Physical therapy is often extremely beneficial and frequently overlooked, so finding a good pelvic floor PT to be part of your healing team is key too.

When responding to the blog question I commented that “your friend is fortunate to have you looking out for her”. Using some or all of the above approaches I would expect her to find some relief of the vulva pain, the foot pain and experience reduced anxiety and depression (assuming these are her root causes).

Please note that this is not an exhaustive list of contributing factors for vulvoldynia – other factors could include candida, infections such as HPV, IBS/SIBO, and trauma and sexual abuse. My colleague, Jessica Drummond, nutritionist and physical therapist, and an expert on female pelvic pain, writes about immunity, dysbiosis, gluten and other food sensitivities, cortisol and sex hormone imbalances in this article: Vulvovaginal Pain and The Immune System: Practical Steps for Vulvovaginal Pain Relief. A full functional workup is required and your root cause can be different from someone else’s root cause.

I’d also like to add that although dietary oxalates cause excruciating pain in my feet, I’m so fortunate, in that I do not have vulvodynia.

Have you had success with a low oxalate diet and calcium citrate for vulvodynia? And other pain (in the feet or hips or elsewhere in the body)?

Has physical therapy with a pelvic floor specialist helped?

Have you found tryptophan, GABA or DPA to help with the pain and the anxiety and/or depression too?

Have any other treatments helped you?

If you’re a practitioner what approaches have helped your clients/patients?

Please share questions or feedback below.

 

How do I taper from my antidepressant with tryptophan and can I safely use the other amino acids?

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antidepressant-tapering

Today’s article is based on a question I am seeing more and more on the blog: How do I taper from my antidepressant with tryptophan and can I safely use the other amino acids?

I find my clients do better when tapering off an antidepressant (which is often prescribed for anxiety and panic attacks) when their nutritional status is solid. Incorporating diet changes and adding amino acids and other nutrients first can result in a more successful taper with less side-effects. This would mean starting with the basics – eating real whole food, incorporating quality animal protein, eating to balance blood sugar, and removing gluten, caffeine and sugar.

If needed and based on testing results, it’s important to address any other nutritional deficiencies such as low iron, low vitamin D, low stomach acid, low total cholesterol, low B12 (and whatever else is an issue), plus support the adrenals/sex hormones/thyroid if needed and addressing gut health like leaky gut and dysbiosis.

Adding a good copper free multivitamin and often the addition of zinc and vitamin B6, evening primrose oil and possibly fish oil – the latter based on each person’s unique needs.

With antidepressants such as selective serotonin-reuptake inhibitors (SSRIs), I have my clients work with their prescribing doctor and get the approval to add tryptophan (or 5-HTP) 6 hours apart from the SSRI. If they are taking the medication at night they get the approval from their doctor to switch it to the morning, and will take tryptophan (or 5-HTP) at least 6 hours later, mid-afternoon and evening.

If they decide to do both the medication and tryptophan (or 5-HTP), they get a protocol for the SSRI taper for the future. This is important. If you are in too big a rush to start right away, it often causes more issues. It’s also important to make sure you get a very slow taper protocol from your doctor. Some antidepressants are harder to taper (Paxil is notoriously difficult) and they all should be tapered really slowly.

The plan is to start to taper the SSRI once you have been using the tryptophan (or 5-HTP) for at least 4 to 8 weeks and are seeing real benefits by using it. This translates to much much less or none of the following symptoms: anxiety, depression, insomnia, rumination, worry, negative-self-talk, perfectionism, afternoon and evening carbohydrate cravings, PMS, rage or anger.

For some of my clients it’s 3 months before they feel they are ready to taper. This may be because of feedback they have provided based on prior taper attempts and how they are feeling this time. It may also be based on what else is going on in their lives like a stressful work situation. It may also be based on the time of the year: winter is generally not a good time to taper and definitely not if you suffer from increased depression or anxiety in winter.  

The tryptophan (or 5-HTP) is adjusted up as needed while continuing to taper the SSRI.  

The doctor is always kept informed and monitors for the possibility of serotonin syndrome. I learned about the potential concerns about serotonin syndrome when using tryptophan or 5-HTP with an SSRI from Julia Ross, author of The Mood Cure, and so I continue to caution my clients about this.

When I interviewed Dr. Peter Bongiorno in season 4 of the Anxiety Summit (Serotonin and anxiety: tryptophan, 5-HTP, serotonin syndrome and medication tapers), he shared that he is not concerned about serotonin syndrome being an issue with tryptophan or 5-HTP dosed with an SSRI, even if taken at the same time. He cited research that found the combination of tryptophan and SSRI did not result in serotonin syndrome in any of the participants.      

Dr. Bongiorno also uses the same approach to address the basics:

the most important thing is that we really establish all the basics and that they’re in the healthiest place possible.  Because if those aren’t there, if a patient just gets off the medication and we haven’t really done anything to change the underlying reasons why they got to the place where they had the mood issue, in most cases they’re going to go back there again.

Some people need amino acid support in more than just the low serotonin area so we review the amino acid questionnaire and consider trials of GABA and other amino acids too. All this only applies for SSRIs and tryptophan or 5-HTP. The other amino acids can safely be used with SSRIs, and it’s not uncommon to also have low GABA, low endorphins, low catecholamines and low blood sugar and need them all, but it’s still best to discuss them with the prescribing doctor.

We also review all the amino acid precautions.

Some people choose to work with their doctor to taper the SSRI and then add the tryptophan (or 5-HTP) once they have quit the medication. I have found that this makes it much harder to do and more side-effects are seen. With the amino acids you start to get some relief right away and have hope on the first day! They also make it so much easier to quit the sugar, gluten and caffeine without having to use will-power.

In summary, these are my recommendations for doing an SSRI taper with amino acids:

  • doctor’s approval to taper the SSRI and use amino acids
  • address diet and nutritional deficiencies first – before starting to taper
  • work with someone knowledgeable in amino acid use
  • OR educate yourself by

                   (please don’t simply read one or two blogs and jump in to this)

  • use the amino acids from day one to start addressing low levels of all the brain chemicals
  • use the tryptophan or 5-HTP at least 6 hours away from the SSRI

I would like to add that Dr. Brogan shares that coffee enemas help her patients who are doing medication tapers and this is something I plan to start implementing going forward.

Have you used a similar SSRI taper protocol? And how did it work for you? What would you have done differently? And what advice would you give someone contemplating an SSRI taper?

Have you found that coffee enemas have helped?

Medication tapering and withdrawal: an interview with Dr. Kelly Brogan

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mind-of-your-own-meme

I recently had the absolute pleasure of interviewing Dr. Kelly Brogan, holistic women’s health psychiatrist and author of the new bestseller, A Mind of Your Own. I’ve had the section on medication tapering and withdrawal effects transcribed because it’s so valuable.

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Kelly: Now much of my practice is devoted to psychiatric medications tapers. Guess what? I didn’t learn that in my training. There wasn’t a single hour of education on this subject. I have learned how to do this from patients, and really from patients globally who are educating each other and frankly educating physicians about how to engage in a safe and responsible psychiatric medication tapers……

…when you try to taper off a medication after long-term exposure, either because you’re no longer deriving that initial benefit from it, or because something has changes about your life circumstance and you want to try a different kind of healthcare maybe, they you might learn that these are some of the most habit forming medications, I would say habit forming substances, on the planet.

I wouldn’t believe this if I haven’t seen it with my very own eyes, but this is what actually compelled me to put down my prescription pad for good. After I read that book, I began to take patients, or at least offer them the opportunity to taper them off of medication. Even when we did it responsibly, I was essentially running an outpatient rehab. I mean from neurologic symptoms to psychiatric symptoms, physical symptoms, autoimmune diseases flaring, patients developing impulsive behavior and even violence. It was beyond description.

Then I began to see that actually a lot of patients around the world are talking about this. They’re talking about withdrawal from anti-depressant specifically, but of course other medications as well. Their doctors are totally ill-equipped to help them because we don’t learn about how to do this in our training. We actually in fact dismiss patients when they talk about these being addictive medications. Of course, now finally Fava is a group of researchers who have finally begun to publish the reality of this withdrawal syndrome, and how disabling it can be.

Since I have 4 grounded lifestyle interventions, and actually begun with nutrition such that I don’t even begin a medication taper until about 2 months into lifestyle change, everything is different now in my practice. I feel that once you can optimize your physiology, you really put yourself in a much, much better position to safely and strategically taper. Wow. Isn’t that something you would want to know before taking your first prescription? I certainly never told any patients that it could be like a horror show and you might never be able come off of a psychiatric medication if you’re taking it for longer than a year or so. I never informed patients of that.

A lot of what I discuss and describe in this book is in service of presenting people with a full picture of what the science has to say before they make a decision. I think we really wish that there was a magic pill. We really wish there was a safe effective quick fix. Unfortunately, what is available is really anything but that.

Trudy: Yeah. We want that quick fix. I’ve got a few follow on questions, because this is a lot of good information here. The fact that you see all these problems when people are coming off the meds, is there a time frame, or is that really dependent on each person?

Kelly: It’s very, very dependent on each person. That ends up being the take home that we are talking about. What I like to call end of one medicine. We’re talking about the fact that our levels of biochemical individuality have ever been more relevant than when we’re exploring how we interact with chemicals in our environment, in our pharmaceuticals. We really need to understand that every single person is an individual.

When I taper patients off of meds, I normally do what’s called a test dose decrease, which often is around 20% to 25% of the dose. We come down by that. Again, this is after we’ve done the initial months at least of fairly strict dietary compliance working with relaxation response, doing 20 minutes or more of movement, working on sleep. All of this has to happen first. Then we begin, and so we start with a test dose. If we see in about 2 to 4 weeks that test dose is completely well-tolerated, meaning you don’t even notice the difference, then we probably can work in bigger increments. That’s actually a godsend. These tapers, when we’re working in 10% and less doses, could take literally years.

You want to begin to learn about what your body is capable of bouncing back from. We begin with 25%. If that’s not a pretty picture, then we’ll just scale it back to about 10% of the initial dose, and work with that 10% increment at about every 2 to 4 weeks, sometimes unfortunately slower. The increment and then the speed are 2 variables that we have to learn for each patient.

I don’t know what I would do without a compounding pharmacy. While many of these medications are available in liquid form, and some of them, like Effexor for example, have beads inside a capsule, to be able to tailor and personalize the dosage to each individual patient is wonderful and that I have that option through compounding pharmacy. I work with one in Massachusetts named Johnson Compounding, and they’ve just been a wonderful support over the years to my patients.

Trudy: Wonderful. Very slow and then obviously very individualized. Now I’m very familiar with the effects of benzodiazepines and the slow taper process that’s needed for someone on the anti-anxiety benzodiazepine medication. Would you say that SSRIs can have comparable effects in some people, or are they not as bad as the benzodiazepines?

Kelly: That’s a great question. What we’ve observed in psychiatry is that there’s really been a transition from using benzodiazepine as sort of like a spot treatment to transitioning into using anti-depressants long-term. When I was in my training, the typical gold standard protocol would be to start somebody on both benzodiazepine and anti-depressant, and then taper them off to benzodiazepine and leave on the anti-depressant with the thinking being that benzodiazepine are acknowledged for their habit forming properties and anti-depressants are totally safe.

What we are learning is in fact, that group that Fava runs, with the papers that they’re putting out, they are essentially equating the anti-depressant withdrawal phenomenon to benzodiazepines. In my clinical experience, I would actually argue that SSRIs are worse with long-term exposure. A lot of people at this point, given that it’s been decades since Prozac, have been on these medications for more than 10 years. We’re really talking about a level of habituation that could be challenging to undo. It’s not that I haven’t. I struggled a lot with Klonopin for example. It’s not that I haven’t encountered challenges with benzodiazepines.

A patient in my practice I’m taking off of Lexapro a thousandth of a milligram a month. I’ve never heard of something like that. Heroin, crack, cocaine, oxycontin: show me something that would ever require that. It’s unbelievable. I think it’s at least comparable I would say, and that’s what the literature is beginning to demonstrate, is that there are actually comparable phenomenon, but we really never ever talked about anti-depressants in this way, so it really is a game changing perspective.

Trudy: The fact that you say people are not told that this could be a possibility, and the fact that you’re talking about this and writing about it I think is so important, because people need to know. They would choose not to do this if they did know. I see there is this MA bill going through [correction: being proposed – you can read more here]. It’s about benzodiazepines and people needing to consent to the fact that it’s going to possibly cause them issues. It sounds like we need to do the same with these anti-depressants.

Kelly: Absolutely, 100%.

Trudy: Now, I’ve heard that certain SSRIs are worse than others. I’ve heard that Paxil can be really bad. Have you seen a difference between different medications?

Kelly: Basically we look at half-life of these medications, and we extrapolate from there. Assuming that Prozac would be the easiest, and there are medications like Paxil and Effexor that are more challenging. In my experience, there are 2 ways of discontinuation – the field likes to call it discontinuations issues. The first is acute. It’s within 72 hours of a dose change where you can get brain zaps and headache, and gastrointestinal distress, you feel agitated. The Paxils of the world are much more likely to cause those more immediate withdrawal symptoms.

What I have found is unfortunately there’s no free lunch. There isn’t a medication that actually is effortless to come off for everyone, so that even when you’re on Prozac, for example, for a long period of time, even though it has this long half-life, it should be easy to come off of, in my experience, it can often be challenging as well. These other medications often manifest as second waves. What I have found is almost uncanny – after about 2 months, it’s almost always 6 to 8 weeks after the final dose or after a major dose change. It’s like the other shoe can drop.

You have those immediate withdrawal symptoms, and then about 2 months later, you can begin to have what has historically been categorized as a relapse. This is when your doctor will tell you, “You see, you should have never even tried to go off your medication. You need it for life. Now you know.” That’s what we’re taught to say. In fact, it’s actually a protracted withdrawal phenomenon. Again, this has now been documented that this can occur for unfortunately, I don’t want to scare anyone, it can occur for months and months and even years after the final dose. That being said, there is a medication that spares you from that arm of this problem.

Even I went for years tapering patients off of Wellbutrin and thinking, “Well, this is the easy one. I can even come down by 50% of the dose, and it’s not a problem.” Right now, I have in my practice, a patient who has been completely destabilized coming down by 25 milligrams of Wellbutrin. Again, it’s a very individualized process, and I don’t think that there are any obvious choices in terms of medications that are easier come off of after long-term exposure.

Trudy: Thank you for sharing that. It’s scary, but the good thing is that there are solutions. People on these medications must do the slow taper and make all the changes that you’ve talked about. I’m glad that you mentioned, “Don’t rush into this, make all the food changes.” We’re going to talk about some of the things that you recommend in a second, but get yourself in a better place to start making these changes. If you’re listening to this and you’re thinking, “Oh my gosh. This is terrible.” Don’t go and rush out and just stop. You simply don’t want to stop cold turkey. You want to be working with someone. Then obviously read the book and get resources so you can be in a good place when you’re starting to make these changes.

Kelly: Absolutely. That’s all incredibly important. Yes. Please don’t ever consider just stopping your medication.

Trudy: Absolutely. I have one final question on the medication aspect. You’ve got a small section in the book where you talk about using amino acids are helping people taper, and as you know, my community is very into using the amino acids. I find them very helpful for helping people with mood and anxiety issues. Can you talk a little bit about how you use the aminos and how beneficial you find them when someone is doing this taper?

Kelly: Yes. Absolutely. I am quite certain that there are many, many, many roads to physiologic and psycho spiritual resiliency. I, in no way, intend to position myself as having the answer by any means. I am very much trying to create a space for all of those who are passionate about natural healing, including yourself and our colleagues, because I think that just about everything in the natural health arena offers you the potential for very high yield, very low-risk healthcare.

I certainly don’t consider myself an expert in amino acids and don’t have a fraction of the knowledge that you have about this arena. That being said, I do use them for tapers specifically. If I use supplements I wait after a month of dietary change before introducing any supplements, mostly because I want to, I don’t know, send patients the message of what a single intervention, in terms of lifestyle, what a dietary intervention can do in terms of moving the needle of their health. I often don’t want to cloud the picture with other interventions like even supplements or even detox.

After that period, if it is necessary, I’ll often lead with some of the supplements that I talk about, whether it’s probiotic or glandulars, I use a lot based on my work with the only mentor I’ve ever had, Dr. Nicholas Gonzales. I learned a lot about using glandulars, using specific minerals, using fatty acids, that sort of thing. Well, we’re working with SSRIs. I tend to use tryptophan more often than 5-HTP. I do use tryptophan even in the 3 to 6 gram range before dinner and before bed. I would say that it’s helpful often, not in every case, with a lot of the insomnia specifically. It’s about the worst thing that can happen in the setting of a taper. It’s the kind of insomnia that’s induced by psychiatric medication taper.

I have several tricks up my sleeve, and that’s certainly one of them. Through my own self-education, and again, you may have a more sophisticated perspective on this that when you use 5-HTP or tryptophan for the longest period of time, meaning over a couple of weeks, so you want to balance it out with tyrosine or DL-phenylalanine. If we are using it for a period of time, I might incorporate that. I have found that when I work with Wellbutrin tapers, it’s extremely helpful. Tyrosine and actually an herb called mucuna support dopamine.

Then all of my patients who are tapering – I have them on a blend of amino acids.

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We cover much more than the medication taper and withdrawal and you can listen to the entire interview here:

 

A Mind of Your Own: The Truth about Depression and How Women Can Heal Their Bodies to Reclaim Their Lives is superb, brave, bold, science-based (which I love!) and offers holistic solutions for depression (and anxiety). Get the book from Amazon or better yet, get a copy from your local book store (ask them to get it if they don’t carry it)!

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It launched March 16th and there is a grass-roots effort to share this book widely because of the mainstream media blackout.  Join the grassroots effort and help share this valuable message!

Take a picture with the book and post on social media with #amindofyourown and you can have an impact. You’ll also automatically show up in “hall of fame” on the tagboard.

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You can go and get the first chapter of the book if you’re on the fence (get it here: http://kellybroganmd.com/amindofyourown/?ref=35). After reading the first chapter, I know you’ll want to get the book and join the grass roots effort.

If you already have the book lets us know in the comments what you think.

Feel free to post questions on the blog and please do share your SSRI or benzodiazepine taper and withdrawal story so we can all be better informed.

PS. Both Kelly Brogan and myself will be presenting at the Mindd Conference in Sydney in May. We’ll also be presenting at IMMH/Integrative Medicine for Mental Health Conference in September in Washington DC. Come along to those events, and you can hear Kelly Brogan speak live, and you can hear me speak live as well.