The Millennium-Warrior Angels Foundation 3 year TBI study. This is the definitive lecture on what constitutes a TBI, how to identify and treat it, supported with our evidence on more than 200 documented cases.

1. © 2004-2017 Millennium Lectures “Bringing clinical science to you.”“Bringing clinical science to you.”
A Grouped Knowledge
Presentation
Study Results: 2014-2016
EDUCATE TRAIN TREAT TRACK

2. June 2016
50% greater suicide
rate in military than in
the civilian population!!

3. Where science is being used there is Hope!

4. What is the PTSD Concept?
 PTSD (post-traumatic stress disorder) is a mental
health problem that some people develop after
experiencing or witnessing a life-threatening event,
like combat, a natural disaster, a car accident, or
sexual assault.

5. Then what is TBI?
 The Dept. of Veteran Affairs and the DoD define TBI
as a “traumatically induced structural injury and/or
physiological disruption of brain function as a
result of an external force.”

6. 6
Figure 7.0: There are common elements in the symptomatology associated with
TBI and PTSD which can account for confusion in making the most accurate
diagnosis. We look at PTSD as a 100% psychologically reactive condition that
does not have the physical component that differentiates it from TBI.
PTS is a
Continuum of
untreated TBI.

7. There is an inverse relationship between the level of inflammation and
the level of neurosteroids as there is an inverse relationship between
neurosteroid and symptomatology.
7
- -

9. Combat Trauma Syndrome (CTS) takes into
account all the significant and “insignificant”
traumas that an individual is exposed to in the
course of their (military) life.
You don’t need to be knocked unconscious or even
knocked down to initiate the “silent” but
progressive brain damage (neuroinflammation) that
can take days or years to elicit symptoms that are
always classified as Psychiatric.

10.  Standard training and
operations
 Repetitive Gun fire
 Flash Bang
 Improvised Explosive
Device (IED)
 Controlled entry blasts
 Mortar fire
 Falling down
 Artillery fire
 Carl Gustav/LAW
 Motor Vehicle Accident
 Motorcycle Accident
 Blunt Head Trauma
 Falling or jumping from roof
top(s).
 Parachute jumps
 Hand to hand training
10

11. The 10 Top Symptoms associated with mildTBI:CTS
1. Fatigue ( 100% of patients )
2. Diminished libido.
3. Disturbed sleep patterns. Insomnia.
4. Inattention with difficulty concentrating
5. Impaired memory, faulty judgment, slowed thinking.
6. Depression w/wo Anxiety and Panic Attacks.
7. Irritability with emotional outbursts of Anger.
8. Difficulty switching between two tasks.
9. Alcohol Abuse w/wo Drugs (self-medicating)
10. Increased infections, illnesses, and loss of muscle tone. 11
All associated with
Neuroinflammation
causing Brain
Hormone
dysregulation.

12.  Mood changes (Emotionally Labile).
 Changes in social behavior.
 Changes in personality.
 Diminished Executive Functions.
 Difficulty with problem solving.
 Loss of flexibility in thinking.
 Inability to sequence complex movements.
 Loss of spontaneity in interacting with others.
 Persistence of a single thought (Perseveration).
 Inability to focus on task (Attending).
 Inability to express language (Broca's Aphasia).
12

13.  Increased aggressive behavior.
 Loss of Short term memory.
 Decreasing long term memory.
 Abnormal Libido and Sexual Behavior.
 Difficulty in understanding spoken words.
 Difficulty with verbal ID of objects.
 Difficulty in recognizing faces (Prosopagnosia).
 Inability to categorize objects (Categorization).
 Right lobe damage can cause persistent talking.
13

14.  Problems with reading (Alexia).
 Difficulty with doing mathematics.
 Inability to focus visual attention.
 Difficulties with eye and hand coordination.
 Inability to locate the words for writing.
 Inability to name an object.
 Inability to attend to more than one object at a time.
 Difficulty with drawing objects.
 Difficulty in distinguishing left from right.
 Lack of self awareness and/or surrounding space that leads to
difficulties in self-care.
14

15.  Production of hallucinations.
 Visual illusions - inaccurately seeing objects.
 Defects in vision (Visual Field Cuts).
 Difficulties with reading and writing.
 Difficulty with locating objects in environment.
 Difficulty with identifying colors (Color Agnosia).
 Word blindness - inability to recognize words.
 Difficulty in recognizing drawn objects.
 Inability to recognize the movement of object.
15

16.  Department of Defense data revealed that
from 2000–2011, 339,046 service members
were diagnosed with a mTBI.
 This was 4.2% of the 5,603,720 who served in
the Army, Air Force, Navy and Marine Corps.
Report to Congress on TBI in the USA:
Understanding the Public Health Problem among Current and Former Military Personnel
June 2013

17.  We are realizing that a large number of Iraq and
Afghanistan veterans are returning with diagnoses of
PTSD.
 This is based upon the growing number of visits to
the VA for psychosocial behavioral issues.
 Studies estimate that at least 20-33% of returning
veterans have symptoms of PTSD (mTBI).
The Nation. April 16, 2013

18. 1. Trauma to the body or directly to the skull can
induce neurotrauma.
2. Neurotrauma has two components:
1. Tissue damage, and
2. Neuro-Inflammation
3. The combination of tissue damage and
inflammation causes an alteration in the molecular
biochemistry of the brain which alters the
physiology of neuronal functioning.

19. Molecular changes occur that are not visible on CT, MRI, HDTI, or MEG.
DepressionBi-PolarParanoiaAnger

21. Neuroinflammation and Psychiatric Illness. Journal of Neuroinflammation
2013, 10:43. Souhel Najjar, Daniel M Pearlman2, Kenneth Alper, Amanda Najjar and Orrin Devinsky. Dept.
of Neurology, NY University School of Medicine, New York, NY 10016, USA
 More recently, Neuro-Inflammatory and
immunological abnormalities have been documented
in patients with Classical Psychiatric Disorders.
 Major Depressive Disorder
 General Anxiety Disorders
 Bipolar Disorder
 Obsessive Compulsive Disorder
 Schizophrenia

22.  An increase in oxidative stress leads to
inflammation, which in turn stimulates microglia to
release chemicals that causes damage and
destruction to neurons and neuro-connections
within the brain (neuro-receptors).
 A growing body of evidence suggests that many
psychiatric disorders, MDD, bipolar disorder (BD),
schizophrenia, and autism are associated with
distinct inflammatory mechanisms in the CNS.
The Role of Inflammation and Microglial Activation in the
Pathophysiology of Psychiatric Disorders. G. R. FRIES, et al., Neuroscience.
2015 Aug 6;300:141-54. Center for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The
University of Texas Medical School at Houston, Houston, TX, USA

23. Inflammation after Trauma: Microglial Activation and
Traumatic Brain Injury. ANN NEUROL 2011;. Anil F. Ramlackhansingh, MRCP, David J.Brooks,
MD,DSc, Richard J. Greenwood, FRCP, MD,and David J. Sharp, MRCP, PhD. Et al Centre for Neuroscience, Dept of Medicine,
Imperial College London, Hammersmith Hospital Campus, London, UK; Institute of Neurology, University College London, UK;
MRC Clinical Sciences Centre, Imperial College London, UK; and Neurodis Foundation , CERMEP Imagerie du Vivant, Lyon, France
 Increased microglial activation can be present up to
17 years after TBI.
 This suggests that TBI triggers a chronic
inflammatory response particularly in subcortical
regions.
 This highlights the importance of considering the
response to TBI as evolving over time and suggests
interventions may be beneficial for longer intervals
after trauma than previously assumed.
23

24. Oxidative Stressors
• Reactive Oxygen
• Reactive Nitrogen
• Lipid Peroxidase
Inflammation
• TH1
• Cytokines
• Chemokines
Disruption of BBB
• Hypoxia
• Ischemia
• Cerebral Edema
Excitotoxicity
• Glutamate
• Calcium
Mitochondrial Dysfunction
BAX ► AIF, CytoC.
Cell Death
• Necrosis
• Apoptosis
• Cavitation
• Loss of Brain
Traumatic Brain Injury: Oxidative Stress and Neuroprotection. Antioxidants & Redox Signaling
Vol. 00, N0. 00, 2013. Carolin Cornelius, Vittorio Calabrese, et al.
Disruption of Receptors
• NMDA, Sigma=1
• GABA-α and -β
• AMPA
Neurosteroids
• Deficiencies
• Enzyme Inhibition
• Retarded production

25. Early intervention
to control
inflammation will
promote a more
neuro-permissive
environment
fostering recovery.
25The Infamous Inflammatory component

26. 4. Physical damage to the brain affects the production
of hormonal signaling between the Hypothalamus
and the Pituitary leading to disruption of the
homeostatic mechanisms.
5. Additionally, inflammation alters the brain’s ability
to produce its own hormones; the Neurosteroids
which are made in Glia.
6. The loss of peripheral hormones and the central
Neurosteroids are at the foundation for loss of
cognition and induction of aberrant neurobehavior.

28. Traumatic Brain Injury-Related Hypopituitarism: A
Review and Recommendations for Screening Combat
Veterans. MILITARY MEDICINE, 175, 8:574, 2010. CPT(P) Arthur F. Guerrero , MC USA ; MAJ Abel Alfonso , MC
USA
 Recent civilian data obtained in those sustaining
head injuries, has found a High Prevalence of
Pituitary Dysfunction. Currently (2010), there is no
data available in the military population.
 The authors found that the prevalence of anterior
hypopituitarism secondary to TBI was as high as 30–
80% after 24–36 months.

29. Hypopituitarism Secondary to Head Trauma. The Journal of Clinical Endocrinology &
Metabolism, 2000, 85(4), S. Benvenga, et al. Cattedra e Divisione di Endocrinologia, University of Messina School of
Medicine, 98125 Messina, Italy
0 5 10 15 20 25 30
Infarct of Posterior Pituitary
Stalk Resection
Normal
Infarct of Anterior Pituitary
Hemmorage of Post. Pituitary
Hemmorage of Hypothalamus
Other
Anatomic Lesions of the Pituitary, Stalk, and Hypothalamus at
CT/MRI
Post-Head Trauma Hypopituitarism (PHTH).
8
28
26
24
N
4
2
93%

30. Acute
3 mo
◄Recovery►
Chronic
12 mo
Hormone Deficient 56% 36%
Gonadotropic 32% 21%
Corticotropic 19% 9%
Somatotropic 9% 10% ↑
Thyrotrophic 8% 3%
30
Prevalence of anterior pituitary insufficiency 3 and 12
months after traumatic brain injury. Europe J Endocrinology. 2006; 154(2):259-
65. Schneider HJ; et al. GK. Max Planck Institute of Psychiatry, Clinical Neuroendocrinology Group Kraepelinstr. 10,
80804 Munich, Germany.
SO, how long after a blast trauma does it
take to have your hormones tested? 

31. 31
A Boolean logic search of Google Scholar using “Hormone-X and Depression”
yielded the above results. These were not screened for accuracy.
128,000
157,000
85,600
398,000
23,000
590,000

32.  Open enrollment of 200 Veterans and Active Military
with a history of CTS.
 Pre-requisites: Blast Trauma, labeled PTSD,
Polypharmacy, multiple suicide attempts, and
treatment resistance depression.
 Positive Millennium-Mood Assessment.
Selection Criteria

33.  Millennium Blast Trauma Panel 3624
 Standard biochemical assessment.
 Based upon clinical symptoms and the
biochemical and hormonal testing, an
individualized treatment protocol was
developed.
Protocol

35. 35

36. Hormone Groupings Composition
Growth Factor GH, IGF-1, IGFBP-3
Testosterone and related Free and Total Testosterone DHEA-s,
Estrogens and related Estradiol, Estrone, Pregnenolone, Progesterone
Thyroid Group TSH, Free T4 and T3, reverse T3, TSH Index
Cortisol Group ACTH and Cortisol (morning)
Ancillary Group LH, Prolactin, Insulin, Vitamin D, Insulin.
Inflammatory Markers: IL-6, IL-1β and TNF-α
All needed for a complete and comprehensive evaluation and treatment

37. Pituitary dysfunction after traumatic brain injury. Sorin G. Beca, Brent
Masel, and Randall J. Urban. Traumatic Brain Injury Rehabilitation, Treatment, and Case Management, Third
Edition CRC Press 2010
37
These are tangible, objective, and measurable levels of hormones.
, DHEA-s
, ▲ Insulin
, LH
(Aka Death)
Another Paradigm Shift is in the interpretation of the lab results.

38.  The “normal reference” and “reference ranges” are not
representative of the individual, but of the group used to establish
these ranges (not part of the sample group).
 So, we use the Gender Median as the target level which has always
lead to improvement of the individual, notably more than using the
“within the range” philosophy.
38
10 9015
We maintain all our neurosteroids at their optimal median level and never
above high-normal levels. We always stay physiological.
50

40. 1. Neuroinflammation and
2. Restoring the Neurosteroid balance
to optimal physiological levels.
3. Concurrently removing all
psychotropic agents.

41.  Oral treatment consisting of 80-90% Nutraceuticals
or supplements that address inflammation.
 N-Acetyl Cysteine (NAC)
 Tocopherols (Vitamin E = alpha, delta, gamma)
 Omega-3/6 (Fish Oils = DHA/EPA)
 Alpha Lipoic Acid (ALA)
 Pyrroloquinoline Quinone (PQQ like CoQ-10)
 Quercetin

42. Efficacy of N-Acetyl Cysteine in Traumatic Brain Injury.
Katharine Eakin, et al. Dept of Neurosurgery, Case Western Reserve University School of Medicine, Cleveland, Ohio,
Dept of Anatomy and Anthropology, Sackler School of Medicine, Tel-Aviv University, Dept of Otolaryngology,
Neurobiology, Communication Sciences and Disorders, and Bioengineering, University of Pittsburgh, Pennsylvania, Dept
of Otolaryngology, Spatial Orientation Center, Naval Medical Center San Diego, San Diego, California, Graduate Program
in Neuroregeneration, Taipei Medical University, Taipei City, Taiwan
 We recently conducted, in an active theatre of war, a
study demonstrating that NAC has beneficial effects
on the severity and resolution of auditory, vestibular
and cognitive function sequelae after blast induced
mild TBI (mTBI) in military personnel.
 Works through decreasing oxidative stress, free
radicals, and inflammation.

43. Modulation of inflammation in brain: a matter of fat. Akhlaq A.
Farooqui, et al. Departments of Molecular and Cellular Biochemistry, and Entomology, The Ohio State University,
Columbus, Ohio, USA.
 Vitamin E, Omega-3 (Fish Oils) and NAC inhibit the
generation of prostaglandins, leukotrienes, and
thromboxanes.
 Down-regulation of NfKappaB.
 Not pharmaceutical intervention but Nutraceutical
intervention.

46. No.
#
Mean
Age
Program
Time
History of
Suicide
Medication
Status (%off)
Median
Improvement
57m/1f 39.8 415 Days 2 attempts 90% 73%
Ranges 23-77 YRS 125-1069 Days 1- 6x 4-16 meds 10% - 100%
No. Clomid
(CPC)
Testosterone
(TPC)
Combination
(CPC+TPC)
57/1 47 11 3
58 military individuals, 57 males and 1 female, a variety of traumas(TBI), with
and without PTS, all on multiple medications, multiple suicide attempts, and
disrupted socialization. Average of treatment time 415 days (13.5mos), 90%
off medication with a 73% improvement in overall condition.
91% had a 50%
improvement
in 90 days.

48. Data: % Improvement & Ages
Distribution - Percent Improvement
10% 20 30 40 50 60 70 80 90 100%
4 1 0 0 6 7 13 8 9 9
Population by Age
20s 30s 40s 50s 60s 70s
6 29 13 5 3 2
91% with a 50% or greater response.
Age Group to Percent Improvement
Age 20-29 30-39 40-49 50-59 60-69 70-79
% 77.5 73.8 69.2 67.0 80.0 57.5

49. Year Cost Includes
1st
$5000.00 – $6,500.00 All labs, supplements, and consults.
2nd
$3,500.00 - $4,500.00 All labs, supplements, and consults.
3rd
$2,500.00 - $3,500.00 All labs, supplements, and consults.
The Congressional Budget Office (CBO) reported in 2012
that the average Veteran is getting about $16,000.00 in
medical care – medication expenses per year. These are
the meds that keep an operator off the field preventing
them from doing what they were trained to do. Consider
the cost to train an operative/asset.
Millennium Protocols

50. The End Q &
A

51. Hormones that modulate inflammation
Growth Hormone Vitamin D3 IGF-1
Allopregnanolone Pregnenolone Progesterone
Testosterone Estradiol Cortisol

52. Characterization of interface Astroglial scarring in the human brain
after blast exposure: a post-mortem case series. The Lancet Neurology, 06, 2016: 15:9,
944-953. 2016. Sharon Baughman Shively, Iren Horkayne-Szakaly, Robert V Jones, James P Kelly, Regina C Armstrong,
Daniel P Perl. 2016
Controls
Astroglial Scarring blocks nerve regeneration.
GFAP=glial fibrillary acidic protein
GFAP